MD, PhD, Assistant Professor of Rheumatology – Consultant Rheumatologist

Fondazione Policlinico Universitario A. Gemelli IRRCS – Università Cattolica del Sacro Cuore- Rome, Italy

Email: stefano.alivernini@unicatt.it



Dr. Stefano Alivernini is Assistant Professor in Rheumatology and consultant rheumatologist at the Fondazione Policlinico Universitario A. Gemelli IRCCS – Università Cattolica del Sacro Cuore in Rome (Italy). He undertook his medical degree and specialty training in Rheumatology at the Università Cattolica del Sacro Cuore in Rome and completed his PhD in Clinical Proteomics at the University of Verona. After the subspecialty degree in Rheumatology he took part to the “Inflammatory Arthritis Fellowship Program” during which he did his training, as research fellow, on synovial tissue biopsy and basic and translational science at the Institute of Clinical Immunology of the Academic Medical Centre in Amsterdam and at the Institute of Infection, Immunity and Inflammation of the University of Glasgow. He obatined his master degree on translational medicine in Rheumatology at the University of Trieste. His research activity is mainly focused on Rheumatoid Arthritis and Psoriatic Arthritis with specific interest on synovitis, mechanisms leading to tissue inflammation and its resolution and on biomarkers discovery for personalised medicine in inflammatory arthritis treatment. In particular, his own interests lie in finding biomarkers predicting sustained remission in response to current treatments aiming to develop novel algorithms for personalized medicine for RA and PsA. He is in chief of the synovial tissue biopsy unit (SYNGem) at the Division of Rheumatology of the Fondazione Policlinico Universitario A. Gemelli IRCCS, which is actively involved in translational studies and tissue-driven clinical trials. He is co-chairing the European Synovitis Study Group (ESSG) and he is a member of the Rheumatoid Arthritis Pathogenesis Centre of Excellence (RACE) network in collaboration with the Universities of Glasgow, Newcastle, Oxford and Birmingham. Dr. Alivernini is the President of the young Italian Society of Rheumatology commission (SIRyoung).



Immune tolerance and resolution of inflammation in inflammatory arthritis






PhD Student

UMR 1173 unit, UFR Simone Veil – Santé of Versailles Saint Quentin University – Montigny le Bretonneux, France

Email: amelaitalisaid@gmail.com


Amel is a PhD student in the UMR 1173 unit at, UFR Simone Veil – Santé of the University of Versailles Saint Quentin / Paris Saclay under the direction of Dr Simon Glatigny. More precisely, she works within the “Inflammatory and immune system” team led by Professor Maxime Breban.
Prior to her doctoral studies, Amel completed her undergraduate degree in life science at Versailles University and her master’s degree in inflammation and inflammatory diseases at Paris Cité Universit (inflamex labex).

Her work focuses on the role and dysregulation of conventional dendritic cells during Spondyloarthritis. Her current project demonstrates altered response of dendritic cells to environmental stimuli during Spondyloarthritis and aims to decipher molecular mechanisms leading to these altered responses.



Exploring TLR signaling in DC from HLA-B27 transgenic rat



Spondylarthritis (SpA) is a group of chronic inflammatory disorders with axial and peripheral symptoms. A strong association of SpA with the human leukocyte antigen (HLA) class I molecule B27 has been known for 50 years but the pathogenic role of HLA-B27 remains largely unexplained. Transgenic rats expressing HLA-B27 and human B2-microglobulin (B27-rat) develop clinical manifestations resembling human disease (rat SpA). Previous studies revealed the fundamental role of gut microbiota, antigen-presenting cells (APCs) and CD4+ T cells for the development of rat SpA. Among APCs, conventional dendritic cells (cDCs) can be divided in two different subsets: cDC1 and cDC2. Whereas most cDC1 express the chemokine receptor XCR1 and are involved in immune tolerance, cDC2 promote adaptive immune responses. To study cDCs responses to environmental factors we focused on the role of Toll like Receptor (TLR) ligands mimicking PAMPs from bacteria, viruses and fungi. First, we found that cDC subsets respond to different TLR ligands. Then, HLA-B27+ XCR1+ cDC1 responses to flagellin and LPS were impaired compared to the response of control cDC1. Importantly, the altered HLA-B27+ XCR1+ cDC1 response is already present before rat SpA development and can potentially contribute to SpA onset. Ongoing studies are now focusing on the mechanisms leading to these altered responses with a specific interest to TLR5 expression and trafficking.


Dr Anne-Sophie Bergot is an expert in Immune Regulation & Microbiome at University of Queensland, Translational Research Institute, Brisbane, Australia. She was awarded a Jian Zhou Research Excellence Award in 2017 and promoted to the faculty position of Research Fellow in 2018. She is leading research projects in Spondyloarthritis.

After receiving her PhD on immune regulation in cancer from La Sorbonne Universitas in France, Dr Anne-Sophie Bergot successfully obtained a 3-year fellowship to work on HPV-associated cancers with Professor Ian Frazer. She then continued her journey working on autoimmune diseases with A/Prof. Emma Hamilton-Williams in T1D and her pre-clinical work set the basis for the first-in-human trial of a liposome-based tolerance strategy for type 1 diabetes starting in 2023. Since 2019, mentored by Prof. Ranjeny Thomas, her research interest lies in understanding the role of the gut microbiome in the development of autoimmune arthritis, and how its interaction with immune cells can be exploited to control the progression of the disease.



The role of gut bacteria in the development of Spondyloarthritis


The interplay of IL-23, probiotic and pathobiont bacteria in the pathogenesis of ileitis and spondyloarthritis in the SKG mouse model

Anne-Sophie Bergot1, Ben Cai1, Rabina Giri2, Amy Cameron1, Emily Duggan3, Kai Lim1, Linda Rehaume1, Mark Morrison1, Jakob Begun2, Ranjeny Thomas1

1UQ Frazer Institute, Faculty of Medicine, The University of Queensland, Brisbane, Australia

2Mater Research Institute-UQ, The University of Queensland, Brisbane, Australia

3Translational Research Institute, Brisbane, Australia


Systemic curdlan (1,3-beta-glucan dectin1-ligand)-treated SKG mice develop gram-negative fecal dysbiosis, Crohn’s-like ileitis and spondyloarthritis (SpA). Besides reducing Th17 cells, anti-IL-23 supports goblet cell integrity, corrects dysbiosis, and prevents disease development in these mice. Curdlan-treated BALB/c and germ-Free (GF) SKG mice do not develop SpA. In GF SKG mice colonised with Altered Schaedler flora (comprising Lactobacillus murinus, Parabacteroides sp, Clostridia sp and Mucispirullum sp), fecal abundance of L. murinus significantly expanded 7 days after curdlan and anti-IL-23.

We studied the impact of monocolonisation of BALB/c or SKG mice with probiotic species L. murinus or a potential pathobiont Parabacteroides species on curdlan-induced SpA.

Curdlan-treated monocolonised L.murinus-SKG mice developed IL-23-dependent ileitis but minimal arthritis, Parabacteroides-SKG developed severe IL-23-dependent ileitis and arthritis while L. murinus co-colonised with Parabacteroides sp. attenuated ileitis and arthritis. In L.murinus-SKG mice without curdlan, expression of Il23-p19, grp78, muc2 and tight junction marker ZO-1 were high, abundant mucin separated bacteria from epithelium and some bacteria resided in the villi. In contrast, Parabacteroides-SKG mice had reduced gut barrier fitness with lower expression of Il23, mucin, ZO-1 and claudins. Within 1 week, in L.murinus or Parabacteroides-SKG mice, curdlan triggered gut barrier disruption with loss of goblet cells, increased Il23 and sXbp1 and loss of Muc2 and high bacteria penetration in the villi. Four weeks later, these mice had ileitis, ileal barrier integrity was compromised, and bacterial DNA colocalised with MPO+ neutrophils and IBA-1+ macrophages.

Thus, proinflammatory dectin-1 activation triggers development of ileitis in GF SKG mice colonised with L. murinus or Parabacteroides alone. However, when both bacteria are present, L. murinus with its capacity to stimulate epithelial barrier protective genes and greater mucus production, mitigates the impact of the SKG-pathobiont Parabacteroides. Furthermore, anti-IL23 enhances goblet cell survival and facilitates expansion of L. murinus, reducing pathogenicity of the mucin-degrading Parabacteroides sp.





FRCP, DPhil, Doctor of Medicine, Professor of Experimental Rheumatology

Botnar Research Centre, NDORMS – Oxford University

Consultant Rheumatologist (OUH NHS Foundation Trust)

Email: paul.bowness@ndorms.ox.ac.uk


Paul Bowness is Professor of Experimental Rheumatology at Oxford University, Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Science (2011-present), and Consultant Rheumatologist at the Nuffield Orthopaedic Centre (1999-2022).  He trained in Natural Sciences and then Medicine at Cambridge University and then undertook postgraduate medical training in London. He received a DPhil (PhD) in Immunology from Oxford University in 1993, under the supervision of Sir Andrew McMichael. His principle research interests are in the immunology of Spondyloarthritis.  He has published over 100 peer-reviewed articles in major scientific journals and has written reviews and chapters in textbooks including in the Oxford Textbook of Medicine. He was elected to ASAS in 2009 and was co-president of the International Congress of the Spondyloarthropathies for 2012.



Autoimmunity-associated T cell receptors recognize HLA-B*27-bound peptides




Paul Bowness1, Xinbo Yang2, Lee I. Garner1, Ivan V. Zvyagin3, Michael A. Paley4, Ekaterina A. Komech3, Kevin M. Jude2, Xiang Zhao2, Ricardo A. Fernandes1, Lynn Hassman3, Grace L. Paley3 , Christina S. Savvides2 , Simon Brackenridge1, Max Quastel1, Dmitriy M. Chudakov3, Wayne M. Yokoyama4, Andrew J. McMichael1, Geraldine M. Gillespie1, and Chris Garcia2


The arthritogenic peptide hypothesis proposes that CD8+ T cells, primed by microbial peptides presented by HLA-B*27, subsequently interact with self-peptides bound by HLA-B*27 to drive inflammation in AS/AxSpA.

We isolated orphan T cell receptors (TCRs) expressing a public BV9 T cell receptor (TCR) from blood and synovial T cells in AS and from the eye in HLA-B*27+ ACUT Anterior uveitis. These TCRs showed consistent pairing with AV21 across tissues and demonstrated clonal expansion in the joint and eye. HLA-B*27:05 yeast display peptide libraries were used to identify shared self and microbial peptides, these are recognized by and activate the AS- and AAU-derived TCRs in the context of HLA-B*27:05. 

Structural analysis showed that TCR:peptide-MHC cross-reactivity was rooted in a strikingly shared binding motif utilized by self and microbial antigens that engages the BV9-CDR3I3 TCRs. Different disease-associated microbial antigens trigger this key motif.

These findings support the hypothesis that cross-reacting microbial and autoantigens could play a pathogenic role in HLA-B*27- associated disease.

Affiliations: 1: University of Oxford, Oxford, UK.  2 Stanford University School of Medicine, Stanford, CA, USA.  3 Pirogov Russian National Research Medical University, Moscow, Russian Federation.  4: Washington University School of Medicine, St Louis, MO, USA.  Ref. Nature  2022 Dec;612(7941):771-777.







Professor of Experimental Immunology

Medizinische Klinik 3-Rheumatologie und Immunologie

Erlangen, Germany

Email: bozec.aline@outlook.com


Prof. Dr. rer. nat. Aline Bozec obtained her PhD degree in Biochemistry in 2004 from University Claude Bernard Lyon 1 where she worked on the effects of in utero exposure to environmental factors as endocrine disruptors on male fertility. In 2005 she joined E. Wagner’s Laboratory at the Research Institute of Molecular Pathology (IMP) in Vienna (Austria). Her research focus on the fundamental aspects of AP-1 transcription factors on bone biology. She moved to the CNIO in 2008, as a Staff scientist in E. Wagner’s Laboratory, BBVA Foundation – CNIO Cancer Cell Biology Programme. Since 2012 she joined the Medizinische Klinik 3-Rheumatologie und Immunologie in Erlangen (Germany) as junior professor (Emmy Noether grant) in Osteoimmunologie and then in 2019 as full professor in experimental immune therapy. Her group particularly focused on crosstalk between metabolism, bone homeostasis and inflammation in the basis of immune-mediated diseases, such as arthritis.

The main research focus of the Bozec Lab is to elucidate the cellular and molecular mechanisms altering the bone marrow under disease challenges such rheumatoid arthritis, osteoporosis, and cancer metastasis. Using in vitro and in vivo gain- and loss-of-function murine models, she uncovered very important roles of the immune system in the differentiation of bone cell types such as osteoclasts and osteoblasts. Currently, we are describing the molecular mechanism, by which i) altered transcription factors signaling in immune cells affects adaptive immunity and inflammation, and ii) how hypoxia inducible factors in B-cells controls autoimmunity, infection and bone homeostasis.



Modulation of epithelial intestinal barrier in the pathogenesis of inflammatory arthritis



Clinical observations suggest that intestinal barrier changes are associated with arthritis. Of note, such intestinal barrier changes are highly dependent on oxygen tensions. Upon hypoxia, tissue is responding with rapid induction of the expression of hypoxia-inducible transcription factors (HIFs). In this study, we show that intestinal expression of the transcription factor HIF2α is increased at the onset of arthritis and induces intestinal barrier dysfunction. Inhibition of intestinal HIF2α alleviates arthritis and regulates epithelial barrier integrity by selectively inhibiting the expression of the pore forming protein claudin-15. Surprisingly, HIF1a plays a different role within the gut-joint axis. The CIA induced intestinal epithelial cell death was shown dependent on the transcription factor HIF1α. The epithelial cell death shifted from apoptosis to necroptosis in the absence of HIF1α in IEC, which enhances the onset and clinical score of arthritis. The increased cellular necroptosis is attributed to RIPK3 expression in the absence of HIF1α in IEC. Our findings support the concept of the gut-joint axis and illustrate the connection between intestinal hypoxia and arthritis



MD, PhD, Professor of Rheumatology, University of Versailles-Paris-Saclay

Research Director, Faculty Simone Veil-Santé

Research area: Chronic Inflammation and Immune System

Head of the Department of Rheumatology, Hospital Ambroise Paré,

Boulogne-Billancourt, France

Email: maxime.breban@aphp.fr


Maxime Breban is Director of the Team: Chronic Inflammation and Immune System at Simone Veil-Health Faculty, and Professor of Rheumatology in the Department of Rheumatology of Ambroise Paré Hospital in Boulogne-Billancourt, France.

He trained in Paris Hospital where he acquired his MD degree (1984-1990). His PhD degree was obtained in 1994, after training supervised at the French National Institute for Medical Research. He was a post-doctoral fellow in Harold Simmon’s Research Center at the University of Texas in Dallas, USA, under the supervision of Pr Joel D. Taurog (1990-1993). He worked as a clinical fellow, then Associate Professor of Immunology in Cochin Hopital, Paris (1993-2002). He then joined the Rheumatology Division of Ambroise Paré Hospital, Boulogne-Billancourt, France, as a Professor of Rheumatology (since 2002) and became Head of the Division in 2011. In the mean time, he acted as director of a research team dedicated to chronic inflammation in rheumatic disorders that moved from Cochin Institute to the Faculty of Simone Veil-Santé in 2013.

He splits his time between clinical duties, teaching and research activities. His research is on the Immuno-Genetics of ankylosing spondylitis and related spondyloarthritis (SPA). He has been a Principal Investigator and Coordinator for several clinical and basic research projects. For the past 20 years, he contributed > 100 original papers, and 40 review papers in the field of SPA. He has coordinated a French book on SPA. He received several awards, including the American College of Rheumatology Fellowship award for Excellence in Scientific Research in 1992 and the Guillaumat-Piel Prize from Foundatun for Medical Research in 2018. He has chaired several meetings and scientific groups and has served on the editorial boards of many scientific journals.



Microbiome and axSpA pathogenesis



Microbiota and axSpA pathogenesis

Maxime Breban, MD, PhD

Université Paris-Saclay, UVSQ, Inserm, Infection & inflammation, Montigny-Le-Bretonneux, and Rheumatology Division, Ambroise Paré Hospital, Boulogne-Billancourt, France.

The role of gut microbiota in spondyloarthritis (SpA) has recently become under intense scrutiny, based on long-standing evidence that gut inflammation belongs to the SpA spectrum and that this disease is characterized by a dominant type 3 immune response. A growing number of cross-sectional studies tried to decipher the complexity of gut microbiota in the context of SpA but yielded quite disparate results. In general, they could separate SpA from control samples based on b-diversity and most often showed some degree of dysbiosis in SpA consisting of reduced a-diversity. We will review our own studies using the simplest 16S-rDNA sequencing and the most comprehensive shot-gun sequencing technics. We will discuss how major changes of microbiota composition may reflect the influence of genetic background and some degree of gut inflammation. We will speculate on the pathogenic significance of gut dysbiosis in the context of SpA and on some of its therapeutic consequences.




Chief Scientific Officer

King’s College London – Genomics England Ltd.

London, UK

Email: matt.brown@kcl.ac.uk



Matt Brown is a clinician-scientist who trained initially in medicine and rheumatology in Sydney, Australia before completing a Doctorate of Medicine based at University of Oxford, focusing on genetics of ankylosing spondylitis.  He was appointed Professor of Musculoskeletal Sciences at University of Oxford in 2004.  In 2005 Matt returned to Australia, firstly to University of Queensland, and since 2016, at Queensland University of Technology, where he was Professor and Director of Genomics.  In 2013 he was elected to Fellowship of the Australian Academy of Sciences in recognition for his achievements in genetics research.  In 2019 he moved to King’s College London and Guy’s and St Thomas’ Hospitals NHS Trust to direct their NIHR Biomedical Research Centre, and in 2021 moved to the position of Chief Scientific Officer of Genomics England. He continues to work in genetics of human diseases, with a particular focus on common and rare bone and joint diseases, and in cancer genomics and personalized medicine. He continues to practice rheumatology, with a particular focus on spondyloarthritis. 



Overview on genetic in axSpA




Full Professor of Rheumatology– Director of the Rheumatology Division –

University Hospital of Cagliari

Cagliari, Italy

Email: cauli@unica.it


Alberto Cauli, MD PhD, is Full Professor in Rheumatology at the University of Cagliari, Italy, as well as Director of the Rheumatology Division at the University Hospital. He started his career as a junior doctor in the team of Prof. Alessandro Mathieu, his lifelong mentor, then he spent many years in London at Guy’s and St. Thomas Hospitals, as research fellow of Prof. Panayi (arthritis clinic) and Dr. Hughes (Lupus Clinic), where he got his PhD in Rheumatology from King’s College. Once back in Italy he has settled down in the island of Sardinia (well known to SpA aficionados for the presence of HLA-B*27:09 subtype in the population) focusing his research on spondyloarthritis and connective tissue diseases. Prof. Alberto Cauli is currently fellow of SIR, BSR, ACR, GRAPPA and ASAS.


CHAIRMAN – Session 8 “Innate Immunity”


Full Professor of Rheumatology, University degli Studi della Campania L.Vanvitelli

Head Section of Rheumatology, AOU L. Vanvitelli

Naples, Italy

Email: francesco.ciccia@unicampania.it



Prof. Francesco Ciccia is a MD and phD, specialized in Internal Medicine and Rheumatology for many years involved in research on the immunological basis of systemic autoimmune diseases. His training took place between the University of Palermo (Italy) and the King’s College of London (UK). Currently Prof. Ciccia holds the position of Full Professor of Rheumatology at the University della Campania L. Vanvitelli. The research of Prof. Ciccia is focused on the study of the innate and adaptive immune mechanisms involved in the pathogenesis of Ankylosing Spondylitis, Psoriatic arthritis, Sjogren’s Syndrome and systemic vasculitides. In particular, Prof. Ciccia’s research has clarified many aspects underpinning the immunological bases of gut joint axis in AS patients.


Gut and axSpA: evidence and controversies



MD, PhD, MSc, Rheumatologist, Rheumatology Associate Professor

Department of Clinical Medicine and Surgery, School of Medicine and Surgery, University of Naples “Federico II”

Naples, Italy

Email: lv.costa@libero.it



Luisa Costa received her MD degree in 2004 and her Rheumatology degree in 2009, both from the University of Naples Federico II, Naples, Italy.

In 2010, she has been Research Fellow at Royal National Hospital for Rheumatic Diseases NHS Foundation Trust, Bath, United Kingdom.

She received her PhD in Medical, Clinical, and Experimental Sciences in 2016, from the University of Padova, Italy.

From December 2013 to May 2022, she has been Assistant Professor in Rheumatology at the Department of Clinical Medicine and Surgery, University of Naples Federico II, Naples, Italy.

As of June 2022, she is Associate Professor of Rheumatology at Federico II University in Naples.

She has participated in several national and international study Projects and Trials, mainly focused on Psoriatic Arthritis. She has coauthored over 146 peer-reviewed scientific articles in international  peer‐reviewed journals (Source: Pubmed), focused on Rheumatology and in particular on Psoriatic Arthritis.



CHAIR – Session 11 “Young session”


Full Professor of Rheumatology

Hôpital Ambroise Paré – AP-HP ; Université Versailles-Saint-Quentin-en-Yvelines

Boulogne Billancourt, France

Email : felicie.costantino@inserm.fr


Félicie Costantino is Professor of Rheumatology at Versailles Saint Quentin University (France). She obtained a PhD in Genetics from Paris-Descartes University in 2013 and works in the “Infection and Inflammation” Research Unit headed by Prof Maxime Breban.

Her main research topic is spondyloarthritis with a special interest on genetics and genomics. She’s currently working on identifying rare variants associated with SpA by combining familial studies, next-generation sequencing and functional genomics. She previously spent one year in Julian Knight group at Wellcome Trust Centre for Human Genetics in Oxford for a collaborative project investigating the role of regulatory variants in spondyloarthritis.

Key publications:

  • Targeted resequencing of the 13q13 spondyloarthritis-linked locus identifies a rare variant in FREM2 possibly associated with familial spondyloarthritis. Mambu Mambueni H et al. (2022). Joint Bone Spine
  • A family-based genome-wide association study reveals an association of spondyloarthritis with MAPK14. Costantino F et al. (2017) Ann Rheum Dis, 76:310-314.
  • Whole-genome single nucleotide polymorphism-based linkage analysis in spondyloarthritis multiplex families reveals a new susceptibility locus in 13q13. Costantino F. et al (2016) Ann Rheum Dis, 75, 1380-1385.
  • ERAP1 gene expression is influenced by non-synonymous polymorphisms associated with predisposition to spondyloarthritis. Costantino F. et al (2015) Arthritis Rheumatol, 67, 1525-1534.



Exploring rare variants in multicase famiilies


Identification of rare variants associated with SpA in multicase-families


Costantino F1

1 UMR1173 Infection & Inflammation (INSERM – Paris Saclay University); Rheumatology department Ambroise Paré Hospital (AP-HP); France


Spondyloarthritis (SpA) is characterized by a high familial aggregation, highlighting the existence of a strong genetic background. Besides HLA-B2, almost 50 other SpA-associated loci have been identified to date. However all these loci explain less than 30% of the disease heritability. Several hypotheses have been proposed to explain this missing heritability, including rare variants involvement. This “common-disease – rare variants” hypothesis led to a renewed interest in family-based designs, probably more powerful than case-control studies to identify rare variants.

During this talk, results of studies combining family-based design and next-generation sequencing in SpA will be detailed. Specific challenges related to rare variant association analysis will also be discussed. Finally, preliminary results of a large whole-genome sequencing study including 378 individuals with SpA from 68 multicase-families will be presented.





MD, MSc, PhD

Full Professor of Rheumatology, Head of Rheumatology Unit

Fondazione Policlinico Universitario Agostino Gemelli IRCCS – Università Cattolica del Sacro Cuore

Rome, Italy

Email: mariaantonietta.dagostino@unicatt.it


Maria Antonietta D’Agostino, MD, PhD is Professor of Rheumatology at Università Cattolica del Sacro Cuore in Rome and Head of Rheumatology Department since August 2020, and previously Professor of Rheumatology at Versailles-Saint-Quentin University in France. 

She is an Honorary Professor at Leeds Institute of Rheumatic and Musculoskeletal Medicine at Leeds University, UK.

Her major research interest is the methodological validation of imaging techniques especially ultrasound as outcome measurement instruments in inflammatory and degenerative rheumatic and muscoloskeletal diseases.

She engages in a wide range of research, ranging from methodological and proof-of-concept approaches through to large national and international clinical trials.

She has published several major papers in the field. 

Professor D’Agostino is OMERACT Executive Member, mentor of the OMERACT Ultrasound Group and Imaging and Biomarker Lead. She served as Chair of the EULAR Standing Committee on Musculoskeletal Imaging from 2010 to 2014 and she is ongoing member of the GRAPPA Scientific Committee.



The added value of sonography in SpA diagnosis and monitoring




PhD, Professor at Shanghai Jiao Tong University School of Medicine – Director for the Shanghai Immune Therapy Institute

Shanghai, Cina

Email: chendong@tsinghua.edu.cn



Dr. Dong is Professor at Shanghai Jiao Tong University School of Medicine and Director for the Shanghai Immune Therapy Institute. He served as a Professor of Immunology and the Director of the Center for inflammation and Cancer at the University of Texas MD Anderson Cancer Center before his move to China, and also was Dean of Tsinghua University School of Medicine in 2016-2020.

Dr. Dong’s research is to understand the molecular mechanisms whereby immune and inflammatory responses are normally regulated, and to apply this knowledge to the understanding and treatment of infection, autoimmunity and allergy disorders as well as cancer. The work from Dr. Dong’s group has led to the discoveries of Th17 and T follicular helper (Tfh) cell subsets in the immune system and elucidation of their biological and pathological functions.



Th17 cells in Autoimmunity




IL-17, also called IL-17A, is produced by specialized T cells, Th17 and other innate lymphocytes. Th17 cells are important in tissue inflammation and autoimmunity. IL-17 signals through two distinct heterodimeric receptors on keratinocytes to regulate psoriasis-like inflammation. On the other hand, IL-17D produced by epithelial cells, functions to maturation of ILC3, innate Th17-like lymphocytes, via CD93. In the conference, I will discuss on our recent data on the function of IL-17 cytokines in mucosal inflammation and homeostasis. These cytokines serve as important targets in treating immune diseases.




Full Professor of Rheumatology and Immunology

Chair of the Department of Rheumatology and Immunology

Ghent University and VIB Center for Inflammation Research, Ghent University

Ghent, Belgium

Email: Dirk.Elewaut@UGent.be



Dirk Elewaut is a Full Professor of Rheumatology and Immunology and Chair of the Department of Rheumatology and Immunology at Ghent University Hospital, Ghent, Belgium, a European Alliance of Associations for Rheumatology (EULAR) and Federation of Clinical Immunology Societies (FOCIS) centre of excellence. He received his medical degree at Ghent University in 1991 and his PhD in 1997 at the same institution. Following his postdoctoral research at the University of California San Diego and the La Jolla Institute for Allergy and Immunology, CA, USA, he joined the faculty of the Department of Rheumatology at Ghent University Hospital in 2001.

He has published more than 330 scientific publications in leading scientific journals and is Principal Investigator of the Unit of Molecular Immunology and Inflammation of the VIB Center for Inflammation Research at Ghent University. Currently, he serves as Chair of the EULAR Research Center and as a member of the editorial boards of several leading rheumatology journals. He has received several awards including the 2020 Carol Nachman Award. His research interests are centred around translational aspects of immune regulation to combat inflammatory arthritis and associated joint damage, with a special focus on the link between gut and joint disease in Spondyloarthritis.


Mechano-inflammation in axSpA



Clinical professor – Head of Research – Chief consultant, “The Rheumatology Research Unit” 

Dept. of Rheumatology, Odense University Hospital – University of Southern Denmark.

Honary professor: Århus University in “Rational and innovative patient pathways”.

Email: torkell.ellingsen@rsyd.dk




CHAIRMAN – Session 3 “Microbiome”



MD, Rheumatologist – Department of Clinical Sciences and Community Health

University of Milan

Department of Rheumatology and Medical Sciences

Gaetano Pini-CTO Hospital

Milan, Italy

Email: ennio.favalli@gmail.com


Doctor Ennio Giulio Favalli is Rheumatologist at the Department of Rheumatology and Clinical Sciences, ASST G. Pini-CTO, University of Milan, Italy. Having graduated from the University of Milan in 1997, Doctor Favalli trained in rheumatology for 5 years spent at the Department Rheumatology and Clinical Sciences, ASST G. Pini-CTO. Doctor Favalli qualified as a rheumatologist in 2002 with a thesis on the use of infliximab in rheumatoid arthritis.

In 2003 Doctor Favalli took up the position of Rheumatologist at the Department of Rheumatology and Clinical Sciences, ASST G. Pini-CTO, becoming Adjunct Professor of Rheumatology in 2006 and Assistant Professor of Rheumatology in 2022 at University of Milan. In 2010 Doctor Favalli became Head of the Early Arthritis Clinic at ASST G. Pini-CTO.

Doctor Favalli is a member of the board of the Lombardy Rheumatology Network (LORHEN) since 2005 and member of the Scientific Committee of the Gruppo Italiano per lo Studio della Early Arthritis (GISEA) since 2013. He published several peer-reviewed papers in the national and international literature focused mainly on the treatment of inflammatory arthritis.




From patient side: the role of Ixekizumab in patient reported outcomes 




The management of the disease according to a treat-to-target approach has now also become an established strategy in the field of spondyloarthritis (SpA). In this scenario, also due to the characteristics that differentiate SpAs from rheumatoid arthritis, the definition and measurement of the patient’s perception, commonly identified with the so-called patient reported outcomes (PROs), appear even more important. To date, several validated tools for the quantification of pain, impact of the disease on quality of life, disability, fatigue, sleep, and mood disorders have been proposed. The role of interleukin 17 (IL-17) in the pathogenesis of SpA is nowadays well established and the positive effects of IL-17 inhibitors (IL-17is) in control disease activity and anatomical progression of disease-related damage are well known. In contrast, the efficacy of this pharmacological class on improving PROs is less known to date. The data from the randomised controlled clinical trials included in the development program of the most recent IL-17i (ixekizumab) for both axSpA and PsA clearly confirm the drug good efficacy profile on this component as well, with in particular a significant reduction in pain, which leads to a cascading improvement in all other patient-reported parameters. This certainly places ixekizumab as a valid therapeutic option for the treatment of SpAs.



Resident in Rheumatology – University of Campania “L. Vanvitelli”

Naples, Italy

Email: forgiulio97@gmail.com


Giulio Forte attained his master degree in Medicine and Surgery in English course at University of Campania ‘’L.Vanvitelli’’. During his graduation period he spent two years at Sofia University (BG), where he first approached to the world of medical research. He is actually a resident in Rheumatology at University of Campania ‘’L. Vanvitelli’’ in Naples (IT), where he’s engaged in both clinical and laboratory research activities in the group led by Professor Francesco Ciccia. He is involved in different research activities mainly focused on Spondyloarthritis, Systemic Sclerosis and Sjogren Syndrome’’.



IL-24 as biomarkers in axSpA





Interleukin-24 (IL-24), also known as Melanoma Differentiation-associated gene 7, is a novel cytokine belonging to the Interleukin-10 cytokine family. First discovered as a tumour suppressor gene, it subsequently emerged to have suppressive and pro-inflammatory properties. Recent evidence suggests its potential role in immune-mediated rheumatic disorders, particularly in Rheumatoid Arthritis (RA) and Spondyloarthritis (SpA). 
We here present data on the involvement of interleukin-24 in SpA by analyzing by ELISA the circulating IL-24 in four independent SpA cohorts with a particular interest in the association with disease phenotype, response to treatment and radiographic progression. 



BSc, MSc, PhD

Research Associate – Spondyloarthropathies

King´s College

London, United Kingdom

Email: j.garrido@kcl.ac.uk


I am a biomedical scientist with broad experience in pharmacology and immunology of Immune-Mediated Inflammatory Diseases (IMID). My PhD research, at the University of Granada (UGR, Spain), identified the therapeutic mechanism of immunomodulatory tetracyclines in intestinal inflammation. Seeking expertise in resolution pharmacology, I initiated my postdoctoral studies at the Queen Mary University of London (QMUL, UK), studying novel agonists of resolution in collaboration with the pharmaceutical industry. Through my current position with Prof. Matthew Brown, at King’s College London (KCL, UK), I investigate the TCR sequences and phenotype of arthritogenic immunity in ankylosing spondylitis. This work has instilled me a strong interest in: (1) the role of the intestine as the training ground for the immune system, (2) the pathological consequences of altering this process, and (3) the mechanism to heal and resolve inflammation.


Validating the arthritogenic hypothesis: connections between gut and entheseal immunity


CD8 T-cells carrying a shared TRBV9 chain with a highly restricted CDR3 motif have been shown to be expanded in ankylosing spondylitis (AS). We sought to define the associated TCRA usage by these T-cells, and characterise them phenotypically. CD8 T-cells were isolated from peripheral blood from 6 AS patient, and from   from 3 healthy controls and one AS patient.  Single-cell mRNA sequencing was used to characterise their gene-expression, and to obtain the full-length paired TCRA and TCRB sequences.

T-cell clones carrying the AS-associated TCRB-CDR3 motif were identified in all 6 AS cases, and in the enthesis from the AS patient but not in the healthy controls.  TCRβ paired with TRAV21 in all cases. They showed reduced expression of markers related to central memory (CD27), granular cytotoxicity (GZMK, CST7) and some recruitment molecules (SELL, CCR7, CXCR3, CCL5, CCL4), and increased expression of CCR6, AQP3, LTB, S100A4, KLRB1, LGALS3, RORC and IL7R, pointing to an imprinting event related to gut mucosal immunity.

Blood and entheseal CD8 T-cell expansions associated with AS share a restricted usage of TCR and TCR chains, suggestive of their reacting to a common antigenic driver(s).  Gene-expression profiling identify them as effector memory lymphocytes with particular chemoattracting properties.







MD, Professor of Medicine, Rheumatology Fellowship Program Director

Director, Spondyloarthritis research program and Clinic

University of California

San Francisco, USA

Email: Lianne.Gensler@ucsf.edu


Dr Lianne Gensler is a Professor of Medicine at the University of California, San Francisco (UCSF) and Program Director for the Rheumatology Fellowship Program. She directs the Spondyloarthritis clinic and research program at UCSF, where she performs clinical and translational research. Dr. Gensler served as the chair of the Spondyloarthritis Research and Treatment Network (SPARTAN) from 2016-18 and is one of the authors of the ACR/SAA/SPARTAN 2015 and revised 2019 recommendations for the treatment of AS and nr-axSpA She is a member of the ASAS executive committee and was a taskforce member for the 2022 ASAS-EULAR guidelines. She has been honored with the Ira M. Goldstein Teaching Award in Rheumatology, the Spondylitis Association Young Investigator Award, and the UCSF Research Mentoring Award. She has also been inducted into the Council of Master Clinicians at UCSF.




ASAS-Eular recommendations for the management of AxSpA




The 2022 update of Axial spondyloarthritis (axSpA) ASAS-EULAR guidelines for the treatment of axSpA were recently published. The guidelines are based on a systematic literature review and a working group meeting to generate consensus for the overarching principles and recommendations intended to help clinicians make informed decisions about the most appropriate treatments for their patients.

The guidelines recommend that nonsteroidal anti-inflammatory drugs (NSAIDs) be used as first-line treatment for axSpA. If NSAIDs are ineffective, or if the disease is more severe, bDMARDs such as TNF inhibitors or IL-17 inhibitors can be used. The guidelines also suggest that physical therapy and exercise should be part of the treatment plan for all patients with axSpA.

They recommend This reflects managing a phenotype and may miss differences in endotypes.

The guidelines reflect 2 new recommendations, including taking the extra-musculoskeletal manifestations into account when considering treatment options. They additionally recommend reconsidering the diagnosis or considering comorbidities in a patient not responding to treatment.

This presentation will reflect on the current recommendations and consider a research agenda for future directions in axial spondyloarthritis treatment recommendations.





Full Professor of Rheumatology – Head of Immuno-Rheumatology Unit

Policlinico Universitario Campus Bio-Medico

Rome, Italy

Email: r.giacomelli@unicampus.it


CHAIRMAN – Session 6 “Adaptive immunity”



Phd, Associate Professor – University of Versailles Saint-Quentin-en-Yvelines

Scientific Coordinator CYMAGES facility at UFR Santé Simone Veil

Montigny- le-Bretonneux, France

Email: simon.glatigny@uvsq.fr



Simon Glatigny completed his PhD in bone and joint biology at the University of Paris 7 “New pathways of CD4 T cell differentiation during Spondyloarthritits”, under the co-direction of Prof. Maxime Breban and Dr Gilles Chiocchia.

His work focused on the functional characterization of CD4+ T cell subsets, in particular Th17, and their induction by antigen presenting cells during experimental arthritis.
During a long post-doctoral fellowship of 8 years in the United States in the team of Dr Estelle Bettelli at the Benaroya Research Insitute (Seattle, WA, USA), he focused on the mechanisms of migration and control of Th17 cells during multiple sclerosis and its experimental model of experimental autoimmune encephalomyelitis.
Simon Glatigny has been recruited as a lecturer with an INSERM excellence chair in immunology at the UFR Simone Veil – Santé of the University of Versailles in September 2019. He joined the team

 “Inflammatory and immune system” led by Professor Maxime Breban within the laboratory 2I “Infection and Inflammation” (2I, UMR 1173 INSERM/UVSQ). In this team, he studies the mechanisms of pathogenicity of CD4+ T cell subsets, their induction and control during spondyloarthritis and his experimental model: the HLA-B27 transgenic rat. He is also interested in the role of the gut microbiota and its interaction with immune system cells during spondyloarthritis.


DCs and Th17 interaction in B27 transgenic rat




Pathogenicity of IL-17 Producing lymphocytes during Spondyloarthritis


Marie Beaufrère 1,2,3, Manon Jacoutot1,2, Amel Ait Ali Said1,2, Roula Said Nahal 3, Gina Cosentino1,

Gaelle Clavel 4, Luiza M Araujo1,2, Maxime Breban,2,3 and Simon Glatigny1,2


1 UMR1173 Inserm, Université Paris-Saclay, Montigny-le-Bretonneux, France

2 INFLAMEX, Laboratoire d’Excellence, Université Paris Diderot, Sorbonne Paris

Cité, Paris, France

3 Ambroise-Paré Hospital, Rheumatology department, AP-HP, Boulogne-Billancourt, France

4 Inserm UMR1125-Université Sorbonne Paris Nord, Rheumatology Division, Avicenne Hospital (APHP),

Bobigny, France.


Spondylarthritis (SpA) is a group of chronic inflammatory disorders with osteoarticular and extraarticular symptoms, including colitis, highly associated with the human leukocyte antigen (HLA) class I allele HLA-B27. A strong association of SpA with HLA-B27 has been known for 50 years but its pathogenic role remains largely unexplained. Transgenic rats expressing HLA-B27 and human b2-microglobulin(B27-rat) develop clinical manifestations resembling human SpA (rat SpA).

Previous studies revealed that IL-17 and TNF-a are two major cytokines implicated in both SpA and rat SpA. In this study, we aimed to determine which lymphocyte subset(s) produce key proinflammatory cytokines IL-17 and TNF-α during rat SpA, characterize their tissue distribution and test their pathogenicity by transfer in athymic (nude) B27-rats. First, we showed that conventional T cells (CD4+ Foxp3-) and gd T cells were the main producers of both IL-17 and TNF-α and coproduced these cytokines during rat SpA. Importantly, IL-17+Tconv and gd T cells were already significantly expanded in the colon of premorbid B27-rats. Then, we showed that CCR6 was a reliable marker to isolate IL-17+ Tconv cells in rats but not IL-17+ gd T cells. Similar expansion of CCR6+ IL-17+ Tconv cells and IL-17+ gd T cells were observed in SpA patients.

Finally, transfer of HLA-B27+ purified Th17 (CCR6+) – but not Th1 – cells induced SpA symptoms

(arthritis and colitis) in athymic B27-rats, providing the first direct evidence of a specific proarthritogenic role of Th17 cells in SpA. Overall, our study demonstrates that IL-17+TNFa+ Th17 cells are already expanded before disease development and are involved in SpA development. Ongoing experiment will determine if IL-17+ gd T cells are also able to induce rat SpA and will decipher the mechanism leading to the generation of both IL-17+ cells in the colon to identify new therapeutic targets.


Associate Professor of Rheumatology

University of Palermo – A.O. Policlinico “Paolo Giaccone”

Palermo, Italy

Email: giuliana.guggino@unipa.it


CHAIR – Session 4 “The mucosal corner”


President, Canadian Rheumatology Association

Head, Division of Rheumatology, UHN and Sinai Health

Co-Director, Spondylitis Program, UHN, University of Toronto

Immediate Past President, Association of Kerala Medical Graduates

Board Member, Spondyloarthritis Research and Treatment Network, SPARTAN, USA

Clinician Scientist, University Health Network & Mount Sinai Hospital, Toronto

Senior Scientist, Krembil Research Institute, Schroeder Arthritis Institute, Toronto

Associate Professor, Medicine and Rheumatology, University of Toronto

Email: nigil.haroon@uhn.ca



Dr. Nigil Haroon, MD, PhD, is the President of the Canadian Rheumatology Association and is the Head of the Division of Rheumatology at the University Health Network and Sinai Health. He is an associate professor of medicine and rheumatology at the University of Toronto and a Senior Scientist at the Krembil Research Institute and the Schroeder Arthritis Institute, a state of the art research facility in Toronto.

Dr. Haroon is an internationally renowned clinician scientist in the field of Ankylosing Spondylitis (AS). He is well published in this area and has been an invited speaker in several international meetings. Dr. Haroon also serves on the board of the Spondyloarthritsi Research and Treatment Network (SPARTAN) as well as on the Medical and Scientific ADvisory Boards of the Spondylitis Association of America and the Canadian Spondyltis Association. Dr. Haroon has won several awards including the Vanier Scholarship and the Jane Bruckel Award of the Spondylitis Association of America.

Dr. Haroon has a well-established translational research program at the University Health Network, Toronto and is known for his work in functional genomics of AS. He has published paradigm-shifting studies in AS including the first study to show that spinal progression in AS could be reduced with the use of TNF inhibitors. He published one of the largest population based studies in AS including a total of 100,000 subjects/controls and identified a significant increased risk of dying from heart attacks and strokes in AS patients. He identified the role for MIF, an innate immune molecule that can drive both inflammation and bone formation in AS patients.



MIF: a potential therapeutic target in axSpA


President, Canadian Rheumatology Association

Head, Division of Rheumatology, UHN and Sinai Health

Co-Director, Spondylitis Program, UHN, University of Toronto

Immediate Past President, Association of Kerala Medical Graduates

Board Member, Spondyloarthritis Research and Treatment Network, SPARTAN, USA

Clinician Scientist, University Health Network & Mount Sinai Hospital, Toronto

Senior Scientist, Krembil Research Institute, Schroeder Arthritis Institute, Toronto

Associate Professor, Medicine and Rheumatology, University of Toronto

Email: nigil.haroon@uhn.ca



Dr. Nigil Haroon, MD, PhD, is the President of the Canadian Rheumatology Association and is the Head of the Division of Rheumatology at the University Health Network and Sinai Health. He is an associate professor of medicine and rheumatology at the University of Toronto and a Senior Scientist at the Krembil Research Institute and the Schroeder Arthritis Institute, a state of the art research facility in Toronto.

Dr. Haroon is an internationally renowned clinician scientist in the field of Ankylosing Spondylitis (AS). He is well published in this area and has been an invited speaker in several international meetings. Dr. Haroon also serves on the board of the Spondyloarthritsi Research and Treatment Network (SPARTAN) as well as on the Medical and Scientific ADvisory Boards of the Spondylitis Association of America and the Canadian Spondyltis Association. Dr. Haroon has won several awards including the Vanier Scholarship and the Jane Bruckel Award of the Spondylitis Association of America.

Dr. Haroon has a well-established translational research program at the University Health Network, Toronto and is known for his work in functional genomics of AS. He has published paradigm-shifting studies in AS including the first study to show that spinal progression in AS could be reduced with the use of TNF inhibitors. He published one of the largest population based studies in AS including a total of 100,000 subjects/controls and identified a significant increased risk of dying from heart attacks and strokes in AS patients. He identified the role for MIF, an innate immune molecule that can drive both inflammation and bone formation in AS patients.



MIF: a potential therapeutic target in axSpA


Professor of Musculoskeletal Medicine

Norwich Medical School, University of East Anglia

Norwich, United Kingdom

Email: N.Horwood@uea.ac.uk



Nikki Horwood started her career as a bone biologist in Melbourne at St. Vincent’s Institute with Profs Jack Martin and Matt Gillespie investigating cytokine-driven osteoclast formation. In 2000, she moved to the UK to work with Prof Sir Marc Feldmann at the Kennedy Institute of Rheumatology, renowned for the development of new therapeutics for rheumatoid arthritis. She recently moved to Norwich Medical School as Professor of Musculoskeletal Medicine.  Her current research projects investigate bone marrow composition and lytic bone lesion development in multiple myeloma, inflammation-driven disorders in bone repair, and mechanisms of new bone formation in ankylosing spondylitis and osteoarthritis.




Immune-stromal interactions in bone formation




The innate and adaptive immune systems are active participants in bone homeostasis and repair.  In axial spondyloarthritis, aberrant bone formation occurs at sites when inflammation is, or has been, indicating that the infiltration of the immune cells is critical component for bone formation.

Bone harbours multiple macrophage subpopulations, including bone resorbing osteoclasts and osteomacs as bone tissue-resident macrophages. These cells participate in all phases of normal bone healing. Cytokines, including oncostatin M, have been shown to promote osteoblast formation both in vitro and in vivo. Macrophages are major producers of cytokines, and the depletion of macrophages impairs bone formation. Whether macrophage and monocyte interactions with osteoblasts, and their mesenchymal precursors, will either inhibit or promote bone formation depends upon the activation state, or polarisation, of the macrophage. Whilst alternatively activated macrophages are thought to be the most likely candidates to promote bone formation, recent work suggests that inflammatory macrophages are also involved in this process.

Further work is in progress regarding the interaction of monocyte/macrophages and osteoblasts during bone formation, and elucidating their cellular cross talk holds great promise to solve a fundamental problem of aberrant bone formation in axial spondyloarthritis.



Full Professor of Rheumatology – Department of Clinical and Biological Sciences- University of Turin

Director of the Academic Rheumatology Centre – Mauriziano Hospital

Turin, Italy

EULAR President

Email: annamaria.iagnocco@unito.it


Professor Annamaria Iagnocco is a full Professor of Rheumatology and the Director of the Academic Rheumatology Canter at the University of Turin, Italy. She is currently the EULAR President. She is the former Head of the EULAR School of Rheumatology, former chair of the EULAR Standing Committee on Education and Training, former co-chair of the OMERACT Ultrasound Group, Chair of the Ultrasound Study Group of the Italian Society for Rheumatology, Chair of the North Italian Network, and member of several working groups on ultrasound and imaging in rheumatic and musculoskeletal diseases. She is a faculty teacher in the EULAR Sonography Courses and has been an invited speaker at numerous prestigious international and national congresses, conferences, and courses. Her research interests in Rheumatology include education, arthritis, and imaging. She is involved in national and international clinical trials and imaging studies on rheumatic and musculoskeletal diseases. She has authored more than 325 peer-reviewed publications and several books and book chapters. She is a co-Editor of the EULAR Textbook on Ultrasound in Rheumatology and a member of the Editorial Board of prestigious international journals.


CHAIR – Session 9 “Clinical overview 1”



Robert D Inman MD

Professor of Medicine and Immunology University of Toronto
Senior Scientist
Schroeder Arthritis Institute

Toronto, Canada

Email: Robert.Inman@uhn.ca


Dr. Inman completed his undergraduate degree at Yale University, and his medical degree at McMaster University. He did his training in Internal Medicine at Vanderbilt University and his fellowship in Rheumatology at the Hospital for Special Surgery in New York. He completed a Research Fellowship at the Hammersmith Hospital in London. He then moved to the University of Toronto where he was appointed Professor in the Departments of Medicine and Immunology.

He is currently Co-Director of the Schroeder Arthritis Institute, Co-Director of the Spondylitis Program at Toronto Western Hospital, and Deputy Physician-in-Chief for Research at University Health Network. He is Past-President of the Spondyloarthritis Resarch Consoritium of Canada (SPARCC).


CHAIRMAN – Session 5 “Adaptive Immunity”




Department of Rheumatology, University Hospital of Leuven

Leuven, Belgium

Email: alla.a.ishchenko@gmail.com



Comorbidities and metabolic burden in Early PsA: data from prospective METAPSA cohor



Comorbidities in early psoriatic arthritis: Belgian prospective METAPSA cohort

Ishchenko A.1,2, Pazmiño S.2,3, Neerinckx B.2,3, Lories R.2,3, de Vlam K.2,3

1Department of rheumatology, Ziekenhuis Netwerk Atwerpen, Antwerp, Belgium; 2Division of rheumatology, University Hospitals Leuven, Leuven, Belgium; 3Skeletal Biology and Engineering Research Centre, Department of Development and Regeneration, KU Leuven, Leuven, Belgium.


Aim. To investigate prevalence of comorbidities and cardiovascular risk factors (CV RF) in treatment naïve early psoriatic arthritis (ePsA) compared to healthy volunteers and to identify factors that contribute to the metabolic burden of the patients.

Methods. In observational multicenter study from UZ Leuven, we compared clinical, demographic characteristics, CV RFs and comorbidities of newly diagnosed naïve to DMARD-treatment adult patients with PsA to sex- and age matched controls.

Results. EPsA patients (67) were matched to healthy volunteers (61). Majority of ePsA had oligoarticulair disease and 95% had skin involvement, mostly mild. Median (IQR) symptom duration before diagnosis was 0.6 (0.22-2.3) years. EPsA group had above normal BMI, higher than controls (28.2 vs 25.7, Cohen’s d=0.49, p=0.006), higher rate of obesity, abdominal obesity and metabolic syndrome (Table 1). Although overall number of comorbidities was similar in ePsA and in controls, 82% of ePsA and patients had ≥1 CV RFs present at baseline as compared to 38% of healthy volunteers (OR [95%CI]: 1.6 [1.14-2.26], p=0.017) (Figure 1). Patients with ePsA had higher odds of having multiple cardiovascular risk factors (OR [95%CI] 2.1 [1.3-3.2], p<0.001) than the controls. Duration of skin psoriasis had no mediation effect on comorbidities or CV RF in ePsA. Patients with ePsA had higher rate of cardiovascular disease (OR 3.2 [1.1-9.2]) and higher Charlson comorbidity index as compared to controls. Diagnosis of PsA was the strongly associated with the number of comorbidities and CV RF after adjusting for age, sex and BMI. Dyslipidemia was the most prevalent comorbidity in the PsA (64.2% vs 39.3% in controls; OR [95%CI]: 1.6 [1.1-2.3], p=0.008). Rate of insulin resistance, arterial hypertension was similar in ePsA and in controls.

Conclusions. PsA patients have higher comorbidities and cardiovascular burden already at early stages of the disease.  Rates of dyslipidemia, metabolic syndrome, cardiovascular disease and obesity are significantly higher in early PsA population as compared to healthy volunteers. This suggests a bidirectional relationship between metabolic disturbances and PsA.





Table 2   Comorbidities in patients with psoriatic arthritis as compared to age and sex matched controls at baseline


early PsA (n= 67)

healthy controls (n=61)

P value

ODDs ratio

[95% CI]

male gender, n (%)

47 (70.1)

35 (57.4)



age, mean (±SD)

47.9 (±14.3)

45 (±14.2)



Patients with ≥1 comorbidities, n (%)

Patients with ≥2 comorbidities, n (%)

50 (74.6)

35 (52.2)

37 (60.7)

17 (27.9)



0.7 [0.5-1.1]

1.9 [1.2-3.0]

Patients with ≥1 CV RF, n (%)

Patients with ≥2 CV RF, n (%)

55 (82.1)

38 (56.7)

23 (37.7)

16 (26.2)



1.6 [1.14-2]

2.1 [1.3-3.2]

Patients with CV morbidity, n (%)

14 (20.7%)

4 (6.6)


2.3 [0.9-5.6]

Charlson comorbidity index ≥1, n (%)                  

21 (31.3)

4 (6.6)


4.8 [1.7-13.1]

dyslipidemia&, n (%)

dyslipidemia treated

                  dyslipidemia documented

43 (64.2)

14 (20.9)

29 (43.3)

24 (39.3)

7 (11.5)

17 (27.9)




1.6 [1.1-2.3]

presence of metabolic syndrome, n (%)

15 (22.4)

5 (8.2)


2.7 [1.1-7.1]

Obesity (BMI ≥30), n (%)

27 (40.3)

11 (18.3)


2.2 [1.2-4.0]

Abdominal obesity#  n (%)

34 (50.7)

18 (29.5)


1.7 [1.1-2.7]

W/H ratio, mean (±SD)

0.99 (±0.12)

0.91 (±0.14)

< 0.001*


waist/hip ratio

males, mean (±SD)

                females, mean (±SD)


1.02 (±0.12)

0.93 (±0.11)


0.94 (±0.09)

0.87 (±)





Smoking, n (%)

15 (22.4)

4 (6.6)


0.6 [0.4-0.8]

presence of type 2 diabetes mellitus, n (%)

8 (11.9)

1 (1.6)


7.2 [0.9-56.5]

arterial hypertension, n (%)

19 (28.4)

12 (19.7)


0.8 [0.6-1.4]

Smoking, n (%)

15 (22.4)

4 (6.6)


0.6 [0.4-0.8]

Alcohol consumption (≥ 6units/week), n(%)

20 (29.9)

17 (27.9)


0.6 [0.7-1.6]


Figure 1. Comparison of comorbidities (A), cardiovascular risk factors (B), cardiovascular disease(C) and Charlson comorbidity index(D) in early PsA and healthy controls.


A.        Number of comorbidities is significantly higher in early PsA (p= 0.045, chi-sq test).


B.        Number of CV RF is significantly higher in early PsA than in controls (p= 0.011, chi-sq test).



C.        Cardiovascular disease was not significantly different in two groups (p= 0.07, chi-sq test).

D.        CCI is significantly higher in early PsA (p=0.005, chi-sq test).



PhD, FHEA, Senior Research Fellow – Centre for Immunology and Infection Control

Queensland University of Technology

Brisbane, Australia

Email: tony.kenna@qut.edu.au


A/Prof Tony Kenna is a cellular immunologist and a Principal Research Fellow at Queensland University of Technology. His research career has focused on human immunology and identification of novel therapeutic approaches for treatment of immune-mediated diseases including ankylosing spondylitis (AS and systemic sclerosis. The genomics revolution of the last decade has greatly expanded understanding of the genetic architecture of many immune-mediated diseases. A major challenge now is to determine how newly identified genetic variants alter immune cell and immune system function(s). Working closely with leading human geneticists A/Prof Kenna’s research integrates world-first genomic data with cellular and molecular immunology to unravel the key drivers of disease pathogenesis. His work also enriches fundamental knowledge of human immunology. A/Prof Kenna’s lab has established biobank of patient clinical material with which to interrogate altered immune function in immune-mediated diseases.


Functional evaluation of ERAP1 in axSpA


Functional interrogation of ERAP1 in AS

Endoplasmic reticulum aminopeptidase 1 (ERAP1) encoded on chromosome 5q15, trims peptides prior to loading on HLA-Class I for presentation to CD8 T cells. Polymorphisms in ERAP1 are strongly associated with ankylosing spondylitis (AS), implicating altered peptide handling and presentation as prerequisites for autoreactivity against an arthritogenic peptide. Risk variants of ERAP1 enhance peptide trimming activity of the enzyme and inhibition of ERAP1 is considered an attractive novel therapeutic strategy for treatment of AS. However, a recent report suggest loss of ERAP1 promotes ankylosis and contributes to altered immune and microbiome profiles contributing to a state of heightened inflammation. We have used ERAP-/- mice to question these findings. We found no evidence for increased ankylosis in ERAP-/- mice. Furthermore, regulatory T cells populations appears normal in ERAP-/- mice. To understand the impact of ERAP1 variants on the gut microbiome we compared faecal microbial composition of health individuals carrying risk or protective variants of ERAP1. We found that ERAP1 genotype was associated with altered function but not the overall composition in healthy individuals.

Together our data indicate that loss of ERAP1 is not associated with enhanced inflammation or ankylosis.

PHD, Assistant Professor Laboratory of Experimental Rheumatology

Radboud University Medical Center

Nijmegen, the Netherlands

Email: Marije.Koenders@radboudumc.nl


Dr. Marije I. Koenders is biomedical scientist and works as assistant professor of Experimental Rheumatology at the Radboud University Medical Center in Nijmegen, the Netherlands. Her research focuses on the IL-17/Th17 pathway in rheumatic diseases, and the application of novel targeted therapy approaches to modulate inflammation and autoimmunity.



Interleukin 17 inhibitors and the effect on enthesitis and pain in Spondyloarthritis



Interleukin-17 (IL-17) is an important proinflammatory cytokine in rheumatology. IL-17 in the pathogenesis of rheumatoid arthritis has been extensively investigated and interesting insights on IL-17 family members and cytokine interactions have been obtained. In spondyloarthritis, the role of IL-17 has been clearly demonstrated by the success of IL-17 targeting therapies. But what do we know about the cellular origin of this cytokine, its effector cells and its contribution to disease pathogenesis? How does IL-17 contribute to enthesitis and pain? In this presentation the current evidence of the effects of IL-17 on inflammation and tissue damage is discussed.





Postdoctoral fellow – Rheumatology and clinical immunology

Odense University Hospital

Odense, Denmark

Email: Maja.Skov.Kragsnaes@rsyd.dk



I conduct research exploring the interplay between the human microbiota and autoimmune and chronic inflammatory diseases (CIDs) to guide translation into clinical practice. My focus areas are I. whether manipulation of microbiota can be beneficial in the care of CID, and II. whether microbiota characteristics can be used as diagnostic biomarkers and/or drug response predictors. We have previously published the results of the first randomised controlled trial (RCT) investigating the impact of one faecal microbiota transplantation (FMT) upon response to methotrexate in adults with active, peripheral psoriatic arthritis (FLORA trial, NCT03058900; http://dx.doi.org/10.1136/annrheumdis-2020-219511). Currently, we are conducting a new RCT, where we investigate if repeated once-weekly capsule FMT can improve the response to conventional therapy in patients with newly diagnosed, untreated CIDs (FRONT trial; NCT04924270).



Fecal microbial transplantation in axSpA




Faecal microbiota transplantation (FMT) is considered the most efficient method to restore a healthy diversity of the gastrointestinal microbiota. The transfer of faeces containing minimally manipulated communities of micro-organisms from a donor to a recipient has revolutionised the treatment of recurrent Clostridioides difficile infection. FMT may also induce beneficial responses in patients with inflammatory bowel diseases, thereby demonstrating local therapeutic immune-modulating abilities. However, whether manipulation of the intestinal microbiota can treat extra-intestinal, immune-mediated disorders remains to be established.

In this session, we will discuss the clinical implementation and practical use of FMT followed by a presentation of the clinical findings from the FLORA trial (trial registration number: NCT03058900). This trial was a 26-week, double-blind, randomised, sham-controlled trial exploring if one single-donor FMT could be a favourable supplement to methotrexate in active, peripheral psoriatic arthritis. In addition, we will share the preliminary results of our recent investigation based on the FLORA trial cohort exploring dynamics of the intestinal permeability as well as faecal, plasma and urine metabolomic profiles following FMT, and how this related to clinical response. Finally, we will make suggestions for designing future FMT trials and stress the importance of cross-speciality collaboration within this research field.        


PhD Student

INSERM/UVSQ U1173 – UFR Simone Veil, Paris-Saclay University – French National Institute of Health and Medical Research

City: Montigny-le-Bretonneux, France

Email: marc_lauraine@hotmail.fr


Marc Lauraine is a PhD student in Professor Maxime Breban’s team at Paris-Saclay University and French National Institute of Health and Medical Research (INSERM). He’s being supervised by both Professor Maxime Breban and Doctor Luiza Araujo-Krause and is part of the team “Inflammatory and immune system” from the “Infection and Inflammation” (2I) laboratory. His thesis project is to study “the effects of HLA-B27 on the TGFβ pathway in CD4+ T cells” by using the SpA experimental rat model. Before his thesis, just after his master degree in Genetics, Genomes and Evolution, obtained in 2018, Marc worked one year as Project Engineer at the French National Center of Scientific Research (CNRS) at Gif-sur-Yvette. He was interested in bacterial retroelement called Group II Introns, trying to further characterize their unique retro-transposition features by using electronic cryo-microscopy.


How does TGFb affect CD4+ T cell response in axSpA?


Effect of HLA-B27 on the BMP/TGFβ pathway in the context of Spondyloarthritis

Marc Lauraine1, Bilade Cherqaoui1, Luiza Krause1, Maxime Breban1-2

1 INSERM U1173, University of Versailles Saint-Quentin-en-Yvelines

2 Service de Rhumatologie, Ambroise Paré Hospital


Background: Spondyloarthritis (SpA) is one of the most frequent inflammatory rheumatic disease. It comprises a large spectrum of osteo-articular inflammatory disorders sharing anatomo-clinical similarities as well as association with HLA-B27. It affects the spine and sacroiliac joints, frequently combined with peripheral joint arthritis, enthesis and extraarticular manifestations, the most frequent of which are psoriasis, uveitis and inflammatory bowel disease (IBD). The HLA-B27/hβ2microglobulin transgenic rat (B27 rat), a model of SpA develops spontaneously inflammatory disorder resembling human SpA and is mediated by CD4+ T cells, with biased expansion of pro-inflammatory Th17 cells and altered regulatory T cells (Treg) function favored by dendritic cells (DCs). Furthermore, we have observed that naive T cells from B27 rats harbour an intrinsic bias favouring Th-17 differentiation.  Recently, a new model of HLA-B27 transgenic drosophila was generated, enabling to identify the BMP/TGFβ pathway as specifically altered by HLA-B27 expression. Indeed, in this model, HLA-B27 was demonstrated to interact with the Saxophone receptor inducing upregulation of the pathway. An interaction was also shown in SpA patients’ cells between ALK2 (ortholog of Saxophone in mammals) and HLA-B27. Furthermore, SMAD2/3, one of the canonical BMP/TGFβ signal transducer, was shown to be more activated in immune cells from SpA patients than in those from healthy controls. This difference between SpA patients and controls was exacerbated after stimulation with Activin or TGFβ.

Aims: Given the central role of TGFβ in the differentiation of naive CD4+ T cells into both Tregs and Th17 cells and dysfunction of these cells in B27 rat, our major goal was to investigate the impact of HLA-B27 on canonical and non-canonical BMP/TGFβ pathways in CD4+ T cells subsets from premorbid (before disease onset) and adult (after disease onset) B27 rats and from SpA patients. For this purpose, we studied the interaction between BMP/TGFβ receptors and HLA-B27 as well as these BMP/TGFβ receptors expression and that of related genes in mesenteric lymph nodes’ (mLN) CD4+ T cell subsets from B27 rats and SpA patients. 

Material & Methods: In ex vivo experiments, mLN T cells from B27 and non-transgenic (NTG) rats were stained with specific antibodies to identify the different T cell subsets (naive, effector and activated CD4+ T cells) and to analyze the phosphorylation of proteins of the non-canonical TGFb pathway (p38, ERK1/2, AKT, mTOR) and canonical (SMAD2/3) pathways. mLN T cells were isolated and stimulated in vitro for 1 hour with TGFβ and SMAD2/3 phosphorylation was determined in different T cell subsets by intracellular staining. In some experiments, sorted naive or activated CD4+ T cells, were stimulated with TGFβ and the expression of BMP/TGFβ-related genes was assessed by RT-qPCR. The expression of several receptors of BMP/TGFβ pathway was performed by RT-qPCR on sorted naive and effector CD4+ T cells from SpA patients and B27 rats. The interaction of HLA-B27 with both ALK2 and ALK3 receptors was investigated in rats’ lymphocytes from mLN by proximity ligation assay.

Results and Conclusion: The phosphorylation of proteins of the non-canonical (p38 and AKT) and the canonical (SMAD2/3) pathways was lower in naive and effector T cells from B27 premorbid rats compared to NTG controls. After induction with TGFβ, the SMAD2/3 phosphorylation reached similar levels in T cell subsets from NTG and B27 rats. Analysis of TGFβ-induced genes in naive CD4+ T cells demonstrated differences in the expression of several genes (Icos, Foxp3, Tgfb1) between NTG and B27 adult rats. Low Tgfb1 expression was confirmed in naive and effector CD4+ T cells from B27 premorbid rats. Furthermore, as previously shown in human cells, an interaction of HLA-B27 was observed in mLN from rats, with ALK2and also with the ALK3 receptor. Altogether these findings showed differences in TGFβ-signaling in B27 CD4+ naive T cells that could influence its fate/stability and contribute to its proinflammatory profile.


MD, PhD, Rheumatologist

Sint Maartenskliniek (Woerden, Nijmegen)

Woerden and Nijmegen, the Netherlands

Email: E.Leijten@maartenskliniek.nl


Emmerik Leijten was born 19th of January 1984 in Miami, Florida. He went to elementary school in the Netherlands and attended high school in New Jersey, the United States. In 2002 he moved to Groningen to study Medicine at the Rijksuniversiteit Groningen. After finishing Medical School in 2008, he took courses on Medical Anthropology and Sociology at the University of Edinburgh in 2009 and worked as clinician on the Internal Medicine ward of the Diakonessenhuis in Paramaribo, Suriname in 2010. Afterwards he starting his training to become a rheumatologist at the UMC Utrecht. In 2013 he started doing research at the Laboratory of Translational Medicine in the group of prof. dr. Radstake and dr. Boes. He performed translational research on psoriasis and psoriatic arthritis, striving to uncover clinical and immunological questions. In 2021 he completed his PhD thesis entitled “Letting go of the dichotomy between psoriasis and psoriatic arthritis” and in the same year completed his training as a rheumatologist. Subsequently he has worked as rheumatologist at the Sint Maartenskliniek (Woerden and Nijmegen) and continued with research in the field of psoriatic arthritis and spondyloarthritis as part of the research team in the Sint Maartenskliniek. He enjoys teaching medical students, with specific enthusiasm for the field of rheumatology. He has been an invited speaker at congresses, has been a member of the editorial board of a scientific journal and helps supervise medical students and PhD students in the research field of psoriatic arthritis and axial spondyloarthritis. Outside of work Emmerik enjoys football, (fly)fishing and spending time with his family.



Sex differences in treatment efficacy of interleukin 17 inhibitors in Spondyloarthritis


Interleukin 17 inhibitors have proven efficacy for patients with radiographic and non-radiographic axial spondyloarthritis. Recent post-hoc-analysis from multiple large randomized controlled trials have indicated that the response to interleukin 17 inhibitors is significantly lower in female patients as compared to male patients, both in the radiographic and non-radiographic status. These data and other recent publications of real-world datasets will be discussed, which together underscore clear sex differences in the treatment response of biologicals prescribed for axial spondyloarthritis. The specific role of interleukin 17 in explaining the disparate treatment response in axial spondyloarthritis population will be explored, looking at other treatment modes of action and other diseases, to critically place the results from axial spondyloarthritis in perspective. Taken together, this analysis indicates that while multiple factors are likely responsible for the observed phenomenon of lower response in females with axial spondyloarthritis, this appears more pronounced in axial spondyloarthritis than other diseases and could have implications for daily clinical practice. Recommendations for future directions are made to clarify open questions.



Research Fellow

Monash Biomedicine Discovery Institute

Victoria, Australia

Email: jiajia.lim@monash.edu



Dr. Jia Jia Lim’s research is focused on T cell immunity in autoimmune disease. She is currently a research fellow in Monash University, AU. She has used X-ray crystallography and biophysical approaches to explain how T cell receptor (TCR) specifically recognises polymorphic Human Leukocyte Antigen (HLA) molecules in the context of aberrant T cell reactivity.



TCR immunology-Molecular basis of T cell immunity in rheumatoid arthritis




Jia Jia Lim1, Tiing Jen Loh1, Claerwen M. Jones1, Lars Klareskog2, Vivianne

Malmström2, Anthony W. Purcell1, Hugh H. Reid1, Nicole L. La Gruta1 & Jamie


1Infection and Immunity Program & Department of Biochemistry and Molecular

Biology, Biomedicine Discovery Institute, Monash University, Clayton, Victoria 3800,


2Rheumatology Division, Department of Medicine, Karolinska Institutet, Karolinska

University Hospital 17177, Stockholm, Sweden

3Institute of Infection and Immunity, Cardiff University, School of Medicine, Heath Park,

Cardiff, CF14 4XN, UK.

corresponding authors: Jamie.rossjohn@monash.edu

The autoreactive T cell repertoire driving disease activity in rheumatoid arthritis (RA)

includes CD4+ T cells that recognize HLA-DRB1 presenting post-translational

modified (PTM) self-antigens. Some HLA-DRB1 alleles have a shared susceptibility

epitope (SE) associated with increased RA incidence. For example, certain PTM of

self-proteins via citrullination leads to the formation of neoantigens that can be

presented by HLA-DR4 SE allomorphs. However, the interplay between the HLA

molecule, PTM epitope and the responding T cell repertoire remain unclear.

To understand the molecular basis of the citrullinated self-epitope, HLA-DR4, and CD4

T cell receptor (TCR), we synthesized citrullinated peptides (i.e., fibrinogen b, aenolase,

and vimentin, which are found abundantly in joint synovium of RA patient,

and investigated structurally their impact on HLA-DR4 recognition. Using

combinational techniques including transgenic mouse model, FACS analyses,

biochemical analyses and X-ray crystallography, we analysed the CD4+ TCR

repertoire of HLA-DR4 presenting citrullinated epitope, affinities, and structure of

TCRs reactive with citrullinated peptides presented by HLA-DR4. TCR repertoire

analysis revealed a conserved gene usage, while citrullinated antigen-specific

residues, in both mice and humans. Crystal structures revealed duality function of SE

of HLA-DR4 in presenting citrullinated epitope, as well as direct contact with the TCR,

suggest a link to RA.





PhD, Rheumatologist – Assistant Professor of Rheumatology

University of Campania “L. Vanvitelli”

Naples, Italy

Email: dranielmar@gmail.com



Daniele attained his PhD at Centre for Experimental Medicine and Rheumatology at the Queen Mary University of London (UK) and now is a rheumatologist and assistant professor of Rheumatology at the University of Campania “L. Vanvitelli” in Naples (IT) in the group led by Professor Francesco Ciccia. His research is now mainly focused on Spondyloarthritis and mucosal immunology. He previously worked on the involvement of ubiquitination pathways in the pathogenesis of autoimmune.



New mucosal player in axSpA pathogenesis




The microbiome has been implicated in the pathogenesis of several autoimmune and immune-mediated diseases, including Spondyloarthritis (SpA). The interaction between the microbiome and the immune system at mucosal sites has been highlighted in SpA, specifically for the gastrointestinal, lung and periodontal sites, as demonstrated by the activation and the recirculation of gut-derived immune cells. Among the different mucosal immune sites, the cervicovaginal mucosa contributes to maintaining homeostasis with the vaginal microbiome and surveying pathogens. This is of particular relevance to patients differing in terms of disease manifestations based on sex. However, studies exploring the role of mucosal uterine cells and dysbiosis in women with SpA are still lacking. This talk will focus on the possible contribution of vaginal and uterine dysbiosis and subclinical inflammation to the pathogenesis of SpA in women. Preliminary data on uterine inflammation in an animal model of arthritis and analysis of the uterine microbiota in SpA patients will be presented. 
This evidence may pave the way for elucidating the cervicovaginal immune crosstalk in PsA and how this might influence systemic and joint inflammation. 



FRCPI, PhD, Professor of Investigative Rheumatology

Leeds Institute of Rheumatic & Musculoskeletal Medicine

University of Leeds

Email: D.G.McGonagle@leeds.ac.uk



Dennis McGonagle is Section Head of Experimental Rheumatology in the Leeds Institute of Rheumatic & Musculoskeletal Medicine.  He has elucidated the pathogenesis of seronegative inflammatory diseases and defined the central role of the enthesis in joint pathology, including the cytokine-mediated enthesitis theory of synovitis in seronegative spondyloarthropathies in 1998. He runs clinics in immune-mediated diseases and a joint autoinflammatory network and has developed the modern immunological disease-continuum classification of inflammation against self and the MHC-1-opathy concept of SpA associated disease. Professor McGonagle’s group has defined normal human enthesis innate and adaptive immunity, including ILCs, MAITs and gd-T cells in addition to enthesis resident conventional T cells and macrophage and neutrophils with inducible IL-23 protein expression. His other interest is the use of native joint resident mesenchymal stem cells for osteoarthritis therapy.

Professor McGonagle has served on the editorial boards of Arthritis & Rheumatology and Annals of Rheumatic Diseases. He was a member of the Scientific Committee of The European Alliance of Associations for Rheumatology (EULAR), Chair and Co-Chair of two EULAR task forces and a member of the UK Medical Research Council Population and Systems Medicine Board (MRC PSMB). Professor McGonagle has won international prizes for his work, including the Verna Wright Lecture (2018), the Pemberton Lecture Award from the Philadelphia Rheumatism Society (2018), and the Royal Academy of Medicine (Bioengineering) Medal (2019).



Immunopathogenesis of enthesistis in axSpA


 The enthesis is the cardinal lesion in axSpA with virtually all of the pathology outside the SIJ being directly linked to entheseal inflammation.   Large entheses in the spine such as the annulus fibrosis are completely fibrocartilaginous in healthy young people.

Given the avascular and aneural nature of these large structures the initial immunopathology is likely played out in the adjacent vascular bone marrow tissue or the ligamentous soft tissue that has a paucity of vessels or in the more vascular peri-ligamentous tissues.

Microdamge with vascular and accompanying neural ingression is an age-related phenomenon.   In order to get a better handle on axial enthesis immunity, we have characterised the enthesis of the spinous process which has much smaller fibrocartilages at insertions

and accordingly, the immune system is in close juxta-position to the bony anchorage sites.    


Akin to the normal skin and intestine, the normal enthesis also has resident macrophages that can be induced to produce key cytokines including TNF and IL-23.  The normal enthesis spinal peri-entheseal bone has an abundant neutrophil population in keeping with the

fact that this is the site of myelopoiesis.  We also note that the normal peri-enthesis ligamentous tissue has a visible marinating neutrophil pool.   Upon extraction and stimulation these neutrophils also produce IL-23.   The normal enthesis also has a resident population

of plasmacytoid dendritic cells that upon TLR7/9 stimulation produces TNF and type 1 interferons, that is probably relevant to the total body pain experienced after viral illness.

The normal enthesis also contains several resident innate or unconventional lymphocytes including ILC3, at least two major populations of γδ T-cells and also MAIT cells with inducible IL-17 protein expression.    We have noted that the Vd1 γδ T-cell

population lacked IL-23R expression but could be coaxed to produce IL-17A protein.   The description of TNF and IL-17A producing MAITs at the normal enthesis is of special interest given the role of such cells as key IL-17 producers in axial SpA patients.   

Given the link between subclinical gut inflammation and axSpA and the recent experimental demonstration of a gut-enthesis immunocyte axis in health, these findings are especially noteworthy.   

 Finally, the normal enthesis has a resident population of conventional  CD4 and CD8 T-cells that are capable of producing IL-17A and IL-17F and other disease relevant cytokines with the Th17 population representing up to 2% of the population.   There is also cross talk between the immune system and the enthesis stroma

with stroma production of  CCL-20 and IL-8 that provides broad innate and adaptive immune chemoattraction during disease.    The nature of these populations has been confirmed by recent single cell RNAseq Atlas data of the enthesis soft tissue and bone.   The presence of such an immune axis at the enthesis may appear

surprising as unlike the skin, there is no microbiotal challenge.   We conceptualise this normal enthesis immune system as a mechanism of fine tuning tissue repair at sites of intrinsic microdamage.


Full Professor of Rheumatology – Director of the Department of Internal Medicine and Therapeutics

University of Pavia

Head of the Division of Rheumatology – IRRCS Policlinico S. Matteo University Hospital

Director of the Postgraduate School of Rheumatology

Pavia, Italy

Email: c.montecucco@smatteo.pv.it


Carlomaurizio Montecucco is Full Professor of Rheumatology and director of the Department of Internal Medicine and Therapeutics at the University of Pavia, Italy. He is also head of the Division of Rheumatology at the IRCCS Policlinico S. Matteo University Hospital, and director of the Postgraduate School of Rheumatology.

His clinical and translational research activity has been mainly focused on autoantibodies in rheumatoid arthritis and connective tissue diseases, as well as on pathogenesis and treatment of rheumatoid arthritis. He has published more than 500 papers on peer reviewed Journals.

He was appointed President of the Italian Society of Rheumatology in 2007 and member of the Scientific Committee of EULAR in 2009. He served as Dean of the University of Pavia Medical School from 2013 to 2019, and as chairman of the PhD Course in Experimental Medicine. He was also member of two different Scientific Committees of the Italian Ministry of Health.

At present he is member of the board of the Lombardy Institute for research & education (POLIS) and President of the Arthritis National Research Foundation (FIRA).


CHAIRMAN – Session 8 “Innate Immunity”



Rheumatologist, Fondazione Policlinico Gemelli IRCCS

PhD candidate at the Graduate School “Life Sciences and Health”, Paris Saclay University

Gif-sur-Yvette, France

Email: gerlando.natalello@gmail.com


Gerlando Natalello is a Rheumatologist at the Fondazione Policlinico Gemelli IRCCS, Catholic University of Rome and PhD candidate at the Graduate School “Life Sciences and Health” at Paris-Saclay University. His research interest is focused on the study of the link between gut inflamma�on, dysbiosis and rheuma�c diseases through ex-vivo cellular models.



News from the Gut in axSpA




A rupture in homeostasis at the interface between the digestive epithelium and the intestinal microbiota is probably causal in the pathophysiology of Spondylarthritis. In order to study this interface, innovative study models are needed. The particularies of patents, both in terms of their genetic background and their intestinal microbiota, must be integrated into these new models. We have developed a model of organoids from colonic biopsies of patients, which allows the culture and expansion of epithelial cells, as well as the characterization in the basal state and after simulation of the epithelial and inflammatory markers profile through gene expression and immunofluorescence. From these patients-derived cells, we have also developed a polarized bi-compartmental epithelial model on Transwell-type inserts, allowing the simulation of a confluent epithelial monolayer by bacterial compounds of interest obtained from bacterial isolation on patient stool specimens. Ultimately, these developments will make it possible to obtain a Gut- on-Chip type model integrating both epithelial cells, immune cells and live anaerobic bacteria, from patient samples, allowing a more detailed study of the mechanisms involved in the pathophysiology of Spondyloarthritis, as well as applications in personalized medicine.



MD, PhD, Associate Professor Diabetes and Nephrology

University of Exeter

Exter, United Kingdom

Email: R.Oram@exeter.ac.uk


Dr Richard Oram is an Associate Professor of Diabetes and Nephrology and Honorary Consultant in Nephrology at the University of Exeter and Royal Devon University Healthcare NHS Foundation Trust. His research interests and include the study of beta cell loss and pathogenesis of type 1 diabetes, and other related autoimmune diseases. 

Over the last 10 years he developed type 1 diabetes and celiac genetic risk scores (T1D GRS) as a method to easily and cheaply measure genetic risk as a single continuous variable composed of multiple single nucleotide polymorphisms. He has developed prediction and classification models to better predict and classify disease using genetic risk combined with other clinical features and biomarkers. This innovative approach of being able to easily and cheaply tag HLA and non-HLA risk has high translational impact as both a research tool to investigate and better understand the biology of T1D and as a diagnostic test to predict T1D and discriminate T1D from T2D and MODY. Type 1 diabetes and celiac genetic risk scores are now being translated for clinical prediction, population screening and classification in multiple countries.



Polygenic risk score in biomedical research



Dr Oram will discuss the genetic architecture of autoimmune disease with a focus on polygenic risk score generation and clinical application of polygenic scores. Dr Oram will describe development of a type 1 diabetes genetic risk score (T1D GRS) and utility for diabetes classification in individual patients and in large cohort studies. Dr Oram will then discuss the utility and application in predicting future type 1 diabetes, including recent large scale newborn screening studies




University of Campania L. Vanvitelli

Naples, Italy

Email: ileniapantano@gmail.com



My name is Ilenia Pantano and I am a rheumatologist of University of Campania L. Vanvitelli. I graduated in 2011discussing a thesis on the role of pericytes in systemic sclerosis. My passion for rheumatology dates back to 2009 when I started attending the department and discovering the importance of systemic autoimmune diseases. From 2013 to 2018 I was a graduate student at the University of Campania L. Vanvitelli where my passion for spondyloarthritis was born. In fact, I had the opportunity to be a sub-investigator in numerous clinical trials concerning psoriatic arthritis and spondyloarthritis and to be able to publish works in journals with a high scientific impact. My field of research focuses mainly on psoriatic arthritis by evaluating the impact of comorbidities on therapeutic response. Actually, I am the manager of the spondyloarthritis outpatient clinic of the Rheumatology Unit where more than 1000 patients are followed up.



The recognition and management of early PsA: which role for the IL23 inhibitor GuselKumab?




Guselkumab is a new human IgG1λ monoclonal antibody that binds to the p19 subunit on IL-23 to inhibit the intracellular and downstream signaling of IL-23. It is approved for psoriasis (PsO) and in psoriatic arthritis (PsA).

Discover 1 and 2  and COSMOS trials had shown GUS efficacy and safety in patients naïve and bio-experienced. Guselkumab has been demonstrated to be superior to placebo in reaching ACR 20/50/70 at week 52, showing its efficacy in peripheral arthritis of PsA.  GUS is also effective in axial symptoms: BASDAI scores improved from baseline to week 52 in naïve patients and in TNF-experienced. These data are maintained for up to 2 years of GUS.

If GUS is used early in PsA there will be a greater therapeutic response which is associated with a greater slowing in the progression of the radiographic damage. In fact, more early is used GUS, and more patients reached disease remission. In a real-life cohort our group demonstrated that GUS is efficacious in early psoriatic arthritis, so it can be used earlier in the disease.


Associate Professor of Rheumatology, School of Medicine, University “Federico II”

Naples, Italy



Professor Peluso is a rheumatologist and researcher at the Federico II University of Naples, with a primary interest in spondyloarthritis. His research began in the early 2000s under the direction of Professor Raffaele Scarpa and covers two main areas: psoriatic arthritis and enteropathic spondyloarthritis with a combination of epidemiological, clinical research and imaging science. Professor Peluso is a member of the Group for Research and Assessment of Psoriasis and Psoriatic arthritis (GRAPPA) and Italian Society of Gastro-Rheumatology (SIGR). Professor Peluso is a co-founded of the CaRRDs (Cardiovascular Risk in Rheumatic Diseases) study group, a research program on cardiovascular risk in spondyloarthritis patients.





CHAIRMAN – Session 4 “The mucosal corner”



Research Technician – Immunology

Schroeder Arthritis Institute

Toronto, Ontario, Canada

Email: Zoya.Qaiyum@uhnresearch.ca


Zoya Qaiyum is a research technician at the Inman laboratory, Schroeder Arthritis Institute, University Health Network, Toronto Ontario. Her work in basic science research investigates the biological pathways linking gut and joint inflammation in axial spondyloarthritis (axSpA).



Profiling T cell receptor polymorphisms in axSpA



Proteomic, transcriptomic, and T-cell receptor (TCR) profiling of synovial integrin-expressing (InEx) T cells in axial spondyloarthritis (axSpA)


The strong clinical and genetic associations between axial spondyloarthritis (axSpA) and inflammatory bowel disease (IBD) underscore the pathogenic role of the gut-joint axis.  Two compelling hypotheses, the aberrant cellular trafficking hypothesis and the arthritogenic peptide hypothesis, attempt to unravel the complex immune events perpetuating gut and joint inflammation in axSpA patients.

Here, we present an examination of gut-related trafficking molecules in the inflamed axSpA joint as evidence supporting the former hypothesis. Mass cytometry and bulk RNA sequencing on axSpA peripheral blood and synovial fluid mononuclear cell identified a subpopulation of mature CD8+ T cells enriched in axSpA synovial fluids with a distinct integrin expression that we termed as the CD103+CD49a+ integrin-expressing (InEx) cells. These InEx cells further exhibited enhanced GZMB, PRF1, TNFAIP3 and IL-10 transcripts. To address the latter hypothesis, we characterized and compared the TCR repertoire of InEX cells and mature CD8+ T cells from reactive arthritis (ReA) using single cell TCR and RNA sequencing technologies. We found that the InEx TCR repertoire from axSpA patients was less diverse, clonally expanded, demonstrated specific TCR gene usage, and shared similarities with ReA mature CD8+ T cells. These observations highlight the inciting and perpetuating mediators of inflammation in axSpA.



Senior Attending Physician (Leitender Oberarzt) and Head of Outpatient Clinic

Department of Internal Medicine 3, Rheumatology & Immunology,

University Hospital Erlangen and Friedrich-Alexander-University (FAU)

Erlangen-Nürnberg, Germany

Email: andreas.ramming@uk-erlangen.de


Andreas Ramming is senior attending physician of Internal Medicine and Rheumatology at the Department of Medicine 3 – Rheumatology and Immunology at Universitätsklinikum Erlangen, Friedrich-Alexander University Erlangen-Nürnberg in Germany. Dr. Ramming studied medicine in Erlangen and at UCSF San Francisco. After graduation, he worked as postdoc in immunology at Ludwig-Maximilians University (LMU) Munich. Two years later, he joined the Department of Internal Medicine IV at the University of Munich, where he started his postgraduate training in Internal Medicine and Rheumatology. In 2012 he joined Steffen Gay´s lab on epigenetics in Zurich for one year. Afterwards he established his research group in Erlangen and finished his postgraduate training in Internal Medicine and Rheumatology. Andreas Ramming´s scientific work includes the study of inflammatory and fibrotic diseases, particularly the molecular interactions between lymphocytes and fibroblasts. Initially, he investigated T cells and focused on regulation of IL-9. His research work led to the understanding of the immunoregulatory function of IL-9 and identified PU.1 as essential factor for the development of fibrotic diseases. In 2016 he became member of the priority program “Innate Lymphoid Cells”, funded by the German Research Foundation (DFG). Since 2019, he is additional member of the DFG collaborative research centre 1181 “Checkpoints for Resolution of Inflammation” in Erlangen. 2019, he received funding for the ERC-Starting grant “BARRIER BREAK”. BARRIER BREAK aims to identify molecular mechanisms that permit spreading of inflammation from the skin to the joint. Dr. Ramming published several high impact papers in different journals including Nature and Nature Medicine. His scientific work has been honored with several awards, including the Wolfgang Schulze Prize and the Theodor Frerichs Prize from the German Society of Internal Medicine.


Fibroblast Activation Protein (FAP) PET-CT for depicting osteoproliferation in axSpA patient




Fibroblasts are key orchestrators of inflammation. Little is known whether these cells change phenotype during resolution of inflammation. We adopted a method to visualise fibroblast activation during inflammation in humans in vivo, which is based on a fibroblast activation protein (FAP) tracer detected by positron emission tomography (PET). While tracer accumulation was high in active arthritis, it decreased significantly after TNF- and IL-17A inhibition. Biopsy-based scRNA-seq analyses in experimental arthritis demonstrated that FAP signal reduction reflected a phenotypic switch from pro-inflammatory MMP3+/IL6+ fibroblasts (high FAP internalisation) to pro-resolving CD200+DKK3+ fibroblasts (low FAP internalisation). Spatial transcriptomics of human joints revealed that pro-resolving niches of CD200+DKK3+ fibroblasts clustered with innate lymphoid cells (ILC)2, whereas MMP3+/IL6+ fibroblasts were co-localised with inflammatory immune cells. CD200+DKK3+ fibroblasts stabilised the ILC2 phenotype and induced resolution of arthritis via CD200/CD200R1 pathway. Taken together, these data suggest a dynamic molecular regulation of the mesenchymal compartment during resolution of inflammation.



MD, Professor of Medicine

University of Texas Health Science Center

McGovern Medical School

Division of Rheumatology

Houston, Texas (USA)




Biomarkers predictive of clinical response in AxSpA




Research Engineer

Université Paris-Saclay / UVSQ, Faculty of Medicine
Montigny-le-Bretonneux, France

Email: vincent.rincheval@uvsq.fr



I obtained my PhD in 2000 during which I studied cell choice between apoptosis and senescence consecutively to the activation of the oncosuppressors Rb and p53. I then became a research engineer and participated in numerous studies on the relationships between mitochondrial dysfunctions, oxidative stress and cell death. After 10 years, I joined a virology research team in which I studied the organization and functioning of viral factories, which are membraneless liquid organelles that are found in cells infected with mononegavirales (e.g. RSV, Rabies virus, Ebola virus). In 2018, I joined Professor Isabelle Guénal’s laboratory where I am currently working in collaboration with Professor Maxime Breban on the HLA-B27 transgenic Drosophila model.



News from B27 Transgenic Drosophila


Contributors: Vincent Rincheval1, Maxence de Taffin de Tilques1, Aurore Rincheval1, Maxime Breban2 and Isabelle Guénal1

1 Université Paris-Saclay, UVSQ, Laboratoire de Génétique et Biologie Cellulaire, 78000, Versailles, France.

2 Université Paris-Saclay, UVSQ, Inserm, Infection et inflammation, 78180, Montigny-Le-Bretonneux, France.

The class I major histocompatibility complex (MHC-I) allele encoding human leucocyte antigen (HLA)-B27 is the main genetic factor predisposing to ankylosing spondylitis (AS) and the related spondyloarthritis (SpA). Strong association between AS and HLA-B27 was first described 50 years ago but still remains largely unexplained. The canonical function of HLA-B molecules is to present antigenic peptides derived from cytosolic proteins to CD8+ T cells, leading to a cytotoxic response. However, HLA-B27-driven pathogenicity does not implicate CD8+ T cells in HLA-B27-transgenic rat model of SpA, leading to hypothesize that other properties of HLA-B27 could account for its pathogenicity (1). To further address such hypothesis, we recently produced transgenic flies expressing human MHC-I heavy chain associated (HLA-B*27:05) or non-associated (HLA-B*07:02) to the disease, in combination with human 2-microglobulin. Drosophila melanogaster is an invaluable system to understand complex molecular mechanisms. Indeed, many cellular signaling pathways and functions are conserved between mammals and Drosophila. We speculated that this simple experimental live system could be suitable to unravel aberrant functional consequences of HLA-B27/hβ2m expression, which could contribute to its pathogenicity (2). Here, we will discuss recent developments showing that HLA-B27/hβ2m specifically affects Drosophila immunity. We show unexpected outcome revealing alteration of conserved molecular pathways that are both involved in the regulation of immunity in insects and bone formation in mammals

(1) Breban M. et al, Seminar Immunopath 2021; doi:10.1007/s00281-020-00832-x

(2) Grandon B. et al, ARD 2010; doi:10.1136/annrheumdis-2019-215832





Researcher in Rheumatology

University of Palermo

Palermo, Italy

Email: chiararizzo87@gmail.com


I am a Researcher in Rheumatology, currently working at the University of Palermo. My research is mainly focused on the immunopathogenesis of Spondyloarthritis, with a special interest in Psoriatic Arthritis, musculoskeletal ultrasound and ultrasound-guided biopsies applied to rheumatic diseases. During my formation I had the opportunity of attending the Rheumatology Department of the Clinic Hospital of Barcelona, the Biopsy Unit of the Policlinico Gemelli in Rome and the University Paris-Saclay to acquire skills to perform synovial biopsies and main laboratory techniques. I currently participate in several national and international research projects and actively attend the outpatient clinic of my Hospital.



Leaky gut in SpA: focus on ZEB proteins


Possible role of ZEB proteins in the pathogenesis of the “leaky gut” in Spondyloarthritis

Chiara Rizzo1, Lidia La Barbera1, Federica Camarda1, Marianna Lo Pizzo2, Leila Mohamadnezhad2, Stefania Raimondo3, Riccardo Alessandro3, Francesco Ciccia4 and Giuliana Guggino1

1 University of Palermo, Department of Health Promotion, Mother and Child Care, Internal Medicine and Medical Specialties, Rheumatology Section – “P. Giaccone” University Hospital, Palermo, Sicilia, Italy

2 University of Palermo, Central Laboratory of Advanced Diagnosis and Biomedical Research (CLADIBIOR), Palermo, Sicilia, Italy

3 University of Palermo, Department of Biomedicine, Neuroscience and Advanced Diagnostics, Section of Biology and Genetics, Palermo, Sicilia, Italy

4 University of Campania Luigi Vanvitelli School of Medicine and Surgery, Department of Precision Medicine, Napoli, Campania, Italy


Background: ZEB proteins are key players in the process leading to increased gut permeability and inflammation in colorectal cancer. Their presence was even related to the reduction of tight junctions in the ileum and in the development and activation of immune cells  (1, 2).

Aim: To evaluate the presence of ZEB proteins in the gut of Spondyloarthritis (SpA) patients and to assess their response to bacterial stimulation and possible effects on gut permeability.

Methods: Ileal samples from patients (AS, PsA, Crohn) and healthy individuals were evaluated by IHC, IF and qRT-PCR to assess ZEBs expression. The presence of tight junctions was evaluated by PCR. Functional experiments were conducted via stimulation of HC ileal samples with patient-derived bacteria to assess ZEB, tight junctions and cytokines expression. 

Results: ZEBs are expressed in the ileum of CD, PsA and AS and less expressed in HC. CD and AS express more ZEBs compared to PsA. Preliminary functional experiments evidenced a role for SpA-derived gut microbiota in modulating ZEB, tight junctions and proinflammatory cytokines expression.

Conclusion: ZEBs are expressed in SpA ileum, influencing gut permeability and are modulated by gut microbiota, possibly confirming the role of dysbiosis in triggering the inflammatory process behind SpA.


  1. Slowicka, K., Petta, I., Blancke, G. et al. Zeb2 drives invasive and microbiota-dependent colon carcinoma. Nat Cancer 1, 620–634 (2020). https://doi.org/10.1038/s43018-020-0070-2.
  2. Charlotte L. Scott, Kyla D. Omilusik, ZEBs: Novel Players in Immune Cell Development and Function, Trends in Immunology, Volume 40, Issue 5, 2019, Pages 431-446, ISSN 1471-4906, https://doi.org/10.1016/j.it.2019.03.001.



MD, Retired Full Professor of Rheumatology

University “Federico II”

Naples, Italy

Email: profrscarpa@gmail.com


Dr. Scarpa is currently Retired Full Professor of Rheumatology at the University FEDERICO II of Naples. He qualified in Naples in 1975 and completed his postgraduate training both at University of Rome La Sapienza in 1981 and at the University of Leeds (UK) in 1984, under the direction of Professor Verna Wright, the famous English rheumatologist who first developed an interest in spondarthritis field and particularly in psoriatic arthritis.

Professor Scarpa is Member of the Italian Society of Rheumatology and of the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis (GRAPPA Group).

Professor Scarpa has published over 300 peer-reviewed papers, many on the subject of psoriatic arthritis and spondyloarthropathies. His main research interests in psoriatic arthritis include clinical and therapeutic studies;  the development of imaging techniques (ultrasound and MRI) for measuring synovial and/or entheseal inflammation; comorbidities in psoriatic arthritis and more recently the analysis of cellular and cytokine profiles in synovial fluid.

Professor Scarpa is President of the Update on Psoriatic Disease, a traditional meeting in the world of International Rheumatology and the first Edition took place in Procida, on May 2008 .  Already from this first Edition, the program of the Update includes the ceremony of the VERNA WRIGHT PRIZE.


CHAIRMAN – Session 11 “Clinical overview 2”


MD, Professor of Internal Medicine
Head of Department
Department of Medicine 3 – Rheumatology and Immunology Friedrich-Alexander University Erlangen-Nürnberg, Germany

Email: georg.schett@uk-erlangen.de


Georg Schett is Professor of Internal Medicine and since 2006 head of the Department of Medicine 3 – Rheumatology and Immunology at Universitätsklinikum Erlangen, Friedrich-Alexander University Erlangen-Nürnberg in Germany.

Professor Schett graduated from the University of Innsbruck (Austria) in 1994. After his dissertation from medical school, he worked as scientist at the Institute of BioMedical Aging Research of the Austrian Academy of Science in Innsbruck. Two years later, he joined the Department of Medicine at the University of Vienna, where he completed his postgraduate training in Internal Medicine and subsequently in Rheumatology. In 2003 he was promoted to professor of Internal Medicine. Before accepting his position as the chair of the Department of Internal Medicine 3 in Erlangen, he worked as a scientist in the United States of America for one year.

Georg Schett’s scientific work includes a broad spectrum of clinical and immunological issues, particularly the molecular basics of immune-inflammatory diseases. Initially, he investigated the immunology of atherosclerosis and focused on antibody-mediated endothelial cell damage. His research work led to the understanding of the phenomenon of LE-cells in 2007. He was awarded the renowned START Award in 2002 and established a research group for arthritis in Vienna. In 2008, he initiated in collaboration with colleagues the priority program IMMUNOBONE in Germany, funded by the German Research Foundation (DFG). IMMUNOBONE aims to elucidate the interactions between the skeletal and the immune systems. Since 2015, Prof. Schett has led the DFG collaborative research centre 1181 “Checkpoints for Resolution of Inflammation” in Erlangen. Additionally, he is spokesperson of the project METARTHROS, funded by the Federal Ministry of Education and Research, which investigates the impact of the metabolism on arthritis. In 2019, he received funding for the ERC-Synergy grant “4D+ nanoSCOPE Advancing osteoporosis medicine by observing bone microstructure and remodelling using a four- dimensional nanoscope” of which he is spokesperson. 4D nanoSCOPE aims to develop tools and techniques to permit time-resolved imaging and characterization of bone in three spatial dimensions (both in vitro and in vivo), thereby permitting monitoring of bone remodelling and revolutionizing the understanding of bone morphology and its function.
In 2021, Prof. Schett was appointed Vice President Research of Friedrich-Alexander University Erlangen-Nürnberg and also became a Leopoldina member of the National Academy of Sciences of Germany.

Professor Schett’s scientific work has been honored with several awards, including the Carol-Nachman Prize from Wiesbaden. He has published over 920 peer-reviewed papers.



Insight in PsA by imaging


Professor of Internal Medicine
Humanitas University
Milan, Italy

Email: carlo.selmi@hunimed.eu


Carlo Selmi received his MD in 1998 and his PhD in Internal Medicine in 2002, both from the University of Milan. Between July 2005 and december 2014, he was Assistant Adjunct Professor of Medicine at the same Division at UC Davis. Since 2022, he is Full Professor of Internal Medicine at the Humanitas University in Milan; he currently leads the Rheumatology and Clinical Immunology Unit at Humanitas research hospital.

Prof. Selmi has coauthored over 350 peer-reviewed publications with a Scopus H index of 65. His research track is dedicated to organ-specific and systemic autoimmune and chronic inflammatory diseases, including the clinical epidemiology and pathogenetic mechanisms of autoimmune liver disease, connective tissue disease (particularly systemic sclerosis), and psoriatic arthritis.


CHAIRMAN– Session 2 “Genetic”




BSc,MSc, 2nd year PhD student

University Health Network

Toronto, Canada

Email: archita.srinath@mail.utoronto.ca



Archita is a 2nd year PhD student at the University of Toronto’s Faculty of Medicine. She is supervised by Dr. Nigil Haroon and is currently studying the deubiquitinase molecule TRABID in the context of ankylosing spondylitis pathogenesis. She earned her BSc. From McMaster University and her MSc. from the University of Toronto under the supervision of Dr. Haroon. Outside the lab, Archita is passionate about mentorship and science translation.



ZRANB1 in AS pathogenesis




The Deubiquitinase molecule TRABID’s Role in Inflammation and Bone Formation in Ankylosing Spondylitis


Background: Inflammation and new bone formation are important disease mediators in ankylosing spondylitis (AS). Recent studies in mice show that the deubiquitinase molecule TRABID (tumor-necrosis factor receptor-associated factor-binding protein domain) epigenetically controls the expression of IL12/23 through JMJD2D (Jumonji Domain-Containing Protein 2D). Furthermore, TRABID also upregulates EZH2 (Enhancer of zeste homolog 2), a molecule that has been implicated in pro-osteogenic pathways. This study aims to study the functional and clinical relevance of TRABID in AS pathogenesis.



  • TRABID, EZH2 and JMJD2D protein and gene expression was evaluated in AS and healthy control tissue by immunohistochemistry/immunofluorescence and qPCR respectively.
  • THP-1 cells (monocyte cell line) were incubated with lipopolysaccharide (LPS) to stimulate cytokine production and varying concentrations of NSC112200, a small molecule inhibitor of TRABID. Enzyme linked immunosorbent assay (ELISA) was used to detect IL23 production after 24 hours in the supernatant. Finally, western blot was used to evaluate expression of EZH2 and JMJD2D.
  • Splenocytes from 16-week-old SKG mice were isolated and incubated with LPS and varying concentrations of NSC112200. ELISA was used to evaluate TNFa expression after TRABID inhibition.
  • TRABID was knocked down in Saos-2 cells (osteoblast cell line) using siRNAs. Cells were then incubated in an osteogenic induction media for 14 days. RNA was extracted every 3 days to evaluate osteogenic gene expression by qPCR and RNA sequencing. At day 14, calcium mineralization levels were evaluated by Alizarin Red staining.



  • Our results showed that TRABID is significantly upregulated in human AS tissue. TRABID+ cells and gene expression were found to be upregulated in AS gut (n=20/group, p<0.0001), bone marrow (n=5/group, p<0.0001) and synovium (n=10/group, p<0.0001). TRABID was found to be preferentially expressed by CD68+ macrophages in the synovial lining. EZH2 and JMJD2D were also found to be significantly upregulated in the inflamed synovium.
  • THP-1 cells treated with NSC112200 and LPS together showed a marked dose dependent inhibition of IL23 production when compared with cells treated with only LPS (n=6, p>0.0001). Furthermore, TRABID inhibition showed a significant downregulation of both JMJD2D and EZH2 protein levels.
  • SKG mouse splenocytes incubated with NSC112200 dose dependently showed decreased levels of TNFa when compared with cells treated with LPS alone after 24 hours (n=3, p=0.0043).
  • TRABID knockdown by siRNA showed significant suppression of pro-osteogenic genes like SP7, Runx2 and alkaline phosphatase. Moreover, osteoblasts knocked down for TRABID failed to mineralize as evidenced by diminished alizarin red staining. RNA sequencing confirmed pathways related to TGFb signalling, bone remodelling and endochondral ossification were supressed while negative regulation of the immune system was upregulated. Lastly, osteogenic induction media significantly upregulated TRABID expression over time, compared with cells treated with unconditioned growth media (p=0.0027).


Conclusions: Our results show a role for TRABID in both cytokine production (TNFa and IL23) and osteogenesis. Future work will address both downstream mechanisms of TRABID in these processes and evaluate TRABID inhibition in animal models of AS. 





Clinical Research Fellow

Kennedy Institute of Rheumatology

Oxford, United Kingdom

Email: davide.simone@kennedy.ox.ac.uk



Davide Simone is a clinician scientist, currently working Postdoctoral Researcher at the Kennedy Institute of Rheumatology. After completing his doctoral studies in Paul Bowness’ lab, where he studied the immunopathogenesis of T cells in SpA, his current research employs computational tools and systems immunology to understand the immunopathogenesis of inflammatory. In parallel to his research, he works as Rheumatology Clinical Fellow at the Oxford University Hospitals.



Single cell insights into the immunology of axSpA




Single cell genomics has revolutionised our comprehension of the immunopathogenesis of immune-mediated conditions. In Ankylosing Spondylitis (AS)  its application has been mostly focused on peripheral blood and synovial fluid. Yet, AS is a multi-organ disease: sampling other anatomical districts can represent an opportunity to understand disease features like inflammation and damage. Indeed, as shown by the Human Cell Atlas, an integrated, cross-tissue reference would allow to chart the different immune phenotypes across the various tissue, which in AS have varying response to immunotherapies, suggesting that different tissue would have different immune signature. This talk will review published and ongoing studies that have used single cell genomics to understand the disease landscape, and propose that the construction of an AS tissue atlas would aid target discovery, improve our understanding of AS tissue biology and represent a necessary step in the direction of precision medicine.


Junior Group Leader, Experimental Immunology

Institute of Molecular Genetics of the Czech Academy of Sciences

Prague, Czech Republic

Email: ondrej.stepanek@img.cas.cz


Ondrej Stepanek graduated at the Charles University in Biology/Molecular Biology in 2007. Then he performed his PhD research in the field of immune cell signaling at the Institue of Molecular Genetics of the Czech Academy of Science in Prague and graduated in 2011. In 2012-2016 he worked as a postdoctoral scientists in the group of Prof. Ed Palmer at the University Hospital in Basel, where he investigated T-cell antigen receptor signaling. In 2016, he established his independent research group at the Institue of Molecular Genetics of the Czech Academy of Science in Prague. The group studies T-cell related signaling and diversity of T-cell subsets in the context of models of immune-related diseases.



Co-receptors in helper and cytotoxic T cells function


The T cell antigen receptor (TCR) signaling machinery relies on the kinase LCK and CD4/CD8 coreceptors to make critical decisions about T cell fate. Despite many years of research, the precise role of CD4- and CD8-LCK interactions in TCR triggering in vivo has remained unclear. To investigate this issue, we developed animal models that express modified LCK at physiologicals levels to determine how coreceptor-bound LCK contributes to TCR signaling. Our study shows that the function of LCK is determined by the specific coreceptor it is bound to. While CD8-bound LCK is not essential for cytotoxic T cell anti-viral, anti-tumor and autoimmune responses in mice, it does help CD8+ T cells respond to suboptimal antigens in a kinase-dependent manner. On the other hand, CD4-bound LCK is necessary for effective development and function of helper T cells through kinase-independent stabilization of surface CD4. Overall, our research uncovers the role of coreceptor-bound LCK in T cell biology and demonstrates that CD4- and CD8-bound LCK utilize different mechanisms to drive T cell development and effector immune responses.




PhD, Research Fellow Scientist 

Schroeder Arthritis Institute, University Health Network

Toronto, Canada

Email: Michael.Tang@uhnresearch.ca


Dr. Michael Tang is a research fellow scientist at the Schroder Arthritis Institute, University Health Network, Toronto, Canada. He has keen research interests in single cell immune profiling of patients with axial spondyloarthritis (axSpA) using mass cytometry and scRNA/TCR sequencing. He will be summarizing recent advances in the role of cytotoxic T cells (CTL) in axSpA pathogenesis and will be presenting his research on immune exhaustion resistance and CTL dysregulation in axSpA. His work is funded by the Arthritis Society Canada.



Dysregulated CTL Exhaustion in axSpA



CTL Dysregulation in AxSpA


Unresolved, chronic inflammation in the spine and of the sacroiliac joints is a key feature in Axial Spondyloarthritis (AxSpA) and is the precursor to later spinal ankylosis. Yet, the immunological events perpetuating inflammation remain to be defined. The strong genetic association with HLA- B27 suggest involvement of CD8+ cytotoxic T cells (CTLs) in AxSpA pathogenesis. A central role for CTL involvement in AxSpA inflammation is supported by our demonstration of chronically activated CTL with distinctive cytokine and integrin profiles. We hypothesize that a loss of CTL immune homeostasis contributes to autoinflammation in AxSpA. In this context, CTL exhaustion represents a hyporesponsive state that limits CTL effector function that would otherwise cause inflammatory pathologies. Using high dimensional single cell immune profiling techniques, we identified a subset of CTLs overrepresented in synovial fluids of AxSpA patients that co-express classical exhaustion markers (PD-1 & TIGIT) with downregulated CD127 expression. These dysregulated CTLs retain their cytotoxic capacity, resist T cell exhaustion, and potentially exacerbate chronic inflammation in AxSpA. Here, we will review genetic and immunological evidence that support the emerging role of CTLs in AxSpA pathogenesis and discuss how dysregulation in T cell exhaustion may sustain chronic inflammation in AxSpA.


MD, PhD, Head of Rheumatology Unit

San Giovanni Bosco, Hospital

Ospedale del Mare, Hospital

ASL Napoli 1 Centro

Naples, Italy

Email: entirri@tin.it



Enrico Tirri is the Head of Rheumatology Unit of San Giovanni Bosco Hospital of Naples, Italy. He teaches in the Specialization School of Rheumatology at the University of Study of Campania “Luigi Vanvitelli”. National Council Member of the Italian Society of Rheumatology (SIR) since 2020. Ordinary Member of Gruppo Italiano di Ricerca in Reumatologia Clinica e Sperimentale (GIRRCS) since 2015. Author of more than 100 papers, of which 25 in indexed international journals, including clinical trial, as principal investigator, about chronic inflammatory arthritis. Speaker and moderator at national and international congresses of Rheumatology. Field of research of his working group: inflammatory arthritis, Sjogren Syndrome, Systemic Lupus Erythematosus.




CHAIRMAN for the Sponsored Lectures


MD, PhD, Professor Rheumatology, Head of the Department of Rheumatology

Radboud University Medical Centre

Nijmegen, the Netherlands

Email: Irene.vanderHorst-Bruinsma@radboudumc.nl



Since 2021 Irene E. van der Horst-Bruinsma is Full Professor in Rheumatology and Head of the department of Rheumatology at the Radboud University Medical Center in Nijmegen, the Netherlands.

Following the completion of her Medical Degree at the University of Leiden in 1987, she was trained in Internal Medicine and Rheumatology at the Leiden University Medical Centre and became a Rheumatologist in 1997. In 1998 she completed her PhD thesis at the Leiden University called “The relationship between HLA Class II polymorphisms and the susceptibility to and progression of  rheumatoid arthritis.” Between 1998-2021 she has been working as a senior staff member at the Rheumatology department of the Amsterdam UMC, location VUmc and is head of the Center of Excellence in Ankylosing Spondylitis. She has supervised over 12 PhD theses and has authored over 300 peer reviewed publications.  In 2018 she was appointed as Professor on sex and gender aspects in musculoskeletal inflammatory diseases at the VU University in Amsterdam.

Prof Irene van der Horst-Bruinsma was member of the Executive Committee of ASAS (Assessment of Spondyloarthritis international society) and is now Advisory Board member of ASAS. She is also member of the EUROSpA steering group, of the IGAS steering committee, the EULAR task Force Gender Equity in Academic Rheumatology (GEAR), Executive Board of the Dutch Society of Gender and Health.  



Sex-specific differences in axSpA: myth or truth?




For many years axial Spondyloarthritis, especially the radiographic subtype, was considered to be a disease with strong male predominance (3:1). However, recent studies have revealed that the disease is also very common in women, especially the non-radiographic subtype (50/50%).  In this presentation many (biological) sex differences between men and women will be discussed, including organ size and function and physiological processes in pain and immune response.

In addition,  the sex differences in disease presentation, diagnosis and response to treatment and drug survival will be presented. Several sex specific challenges in and comorbidity (cardiovascular disease and osteoporosis) will be addressed as well.





PhD, Scientific Coordinator – Principal Investigator Centro Ricerche Fondazione Italiana Ricerca sull’Artrite

Fondazione Pisana per la Scienza & University of Oxford

Pisa & Oxford

Email: m.vecellio@fpscience.it



Dr Vecellio received his PhD degree in Translational and Molecular Medicine in 2012 from the University of Milan – Bicocca (Italy). He has been working in the rheumatology and musculoskeletal disease field since 2013, when he joined the lab of Professor Wordsworth at the Nuffield Department of Orthopedics, Rheumatology and Musculoskeletal Sciences – University of Oxford, working on the genetics of Ankylosing Spondylitis (AS). He has been awarded in 2017 with 5 years Versus Arthritis Career Development Fellowship with a project on the regulation of the transcription factor RUNX3 in AS. He has served as main author in several papers exploring the role of genetic variants associated with AS susceptibility, using a wide array of functional genetics approaches. His lab recent work has been recognized with the Garrod Award 2021- Excellence in Rheumatology Research from the British Society of Rheumatology. From November 2022 he has been appointed as Scientific Coordinator – Principal Investigator of the Centro Ricerche FIRA (Fondazione Italiana Ricerca sull’Artrite) at Fondazione Pisana per la Scienza Onlus. In 2022 he has achieved the National Scientific qualification as associate in Medical Genetics.  




Functional genomics in axSpA




Ankylosing Spondylitis (AS) is a chronic inflammatory arthritis of the spine exhibiting a strong genetic background. The mechanistic and functional understanding of the AS-associated genomic loci, identified with Genome Wide Association Studies (GWAS), remains challenging.  Today, I will show you the recent progress made on the genetic association with AS, with examples covering genome-wide and locus-specific investigation. Further, I will highlight some of the recent techniques we currently use (Chromosome Conformation Capture, Single-cell transcriptomics etc), which are of great help in elucidating a mechanistic explanation for disease-associated genetic variants. A functional genomics approach may ultimately lead to a more precise and comprehensive interpretation of AS association, which is the starting point for emerging and more specific therapies.




Professor of Rheumatology, Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences; Fellow of Green Templeton College

Oxford, United Kingdom

Email: paul.wordsworth@orinst.ox.ac.uk



Professor Wordsworth trained in molecular genetics in the field of single gene disorders affecting the locomotor system. His interests include skeletal dysplasias and Marfan’s disease. He has developed programmes of research into the genetic basis of inflammatory arthritis such as rheumatoid arthritis and ankylosing spondylitis. His clinical interests are in inherited disorders of the skeleton and soft tissues, inflammatory arthritis and autoimmune connective tissue diseases.


CHAIRMAN – Session 1 “Genetic”


Rheumatology clinical Research Fellow, University of Oxford

Rheumatology Specialist Registrar, Oxford University Hospitals

Oxford, United Kingdom

Email: claudia.worth@ndorms.ox.ac.uk








Cytof profiling of blood populations in axSpA


Professor, Chief Physician

Shanghai, Beijing, China

Email: huji_xu@tsinghua.edu.cn


Huji Xu is Professor of Medicine in Second Military Medical University (SMMU) and Tsinghua University

Prof Xu graduated from SMMU where he also completed his residency and internship before he went to Australia to pursue his PhD in rheumatology and clinical immunology. He then worked in Flinders Medical Centre and Queensland Institute of Medical Research. Before he full time returned to China, he was an R.D. Wright fellow of Australian National Health & Medical Research Council and Professor in University of Queensland.

In 2003, Prof Xu has been appointed as a founder chair for the Department of Rheumatology and Immunology at Shanghai Changzheng hospital affiliated to SMMU. His department under his leadership quickly developed into one of the largest clinical and research centres for rheumatology in China. In 2016, Prof Xu has been appointed as founder Executive Dean of School of Clinical Medicine in Tsinghua University.

Prof Xu’s research has encompassed many fields, including rheumatology, human genetics, and vaccinology. Currently, his major research interest is in the area of pathogenesis of rheumatic diseases. His research over last 10 years resulted in several major publications in Nature, Nature Genetics, Lancet Rheumatology, Arthritis & Rheumatism, Annals of the Rheumatic Diseases, Proc Natl Acad Sci USA, The Journal of Experimental Medicine, and Annual Review of Immunology.



Interaction between ERAP-1 and HLA-B27