Reviews
When B cells break bad: development of pathogenic B cells in Sjögren’s syndrome
J.H. Reed1, G.M. Verstappen2, M. Rischmueller3, V.L. Bryant4
- The Garvan Institute of Medical Research, Darlinghurst, and St. Vincent’s Clinical School, Faculty of Medicine, UNSW Sydney, Australia. j.reed@garvan.org.au
- Department of Rheumatology and Clinical Immunology, University of Groningen, University Medical Center Groningen, The Netherlands, and Immunology Division, Walter and Eliza Hall Institute for Medical Research, Parkville, Australia.
- Rheumatology Department, The Queen Elizabeth Hospital and Discipline of Medicine, University of Adelaide, Woodville South, Australia.
- Immunology Division, Walter and Eliza Hall Institute for Medical Research, Parkville; Department of Medicine, The University of Melbourne and Department of Clinical Immunology and Allergy, The Royal Melbourne Hospital, Parkville, and Department of Clinical Immunology and Allergy, The Royal Melbourne Hospital, Parkville, Australia.
CER13769
2020 Vol.38, N°4 ,Suppl.126
PI 0271, PF 0282
Reviews
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PMID: 33025890 [PubMed]
Received: 02/07/2020
Accepted : 29/07/2020
In Press: 22/09/2020
Published: 23/10/2020
Abstract
Primary Sjögren’s syndrome (pSS) is often considered a B cell-mediated disease, yet the precise role of B cells in the pathogenesis is not fully understood. This is exemplified by the failure of multiple clinical trials directed at B cell depletion or inhibition. To date, most prognostic markers for severe disease outcomes are autoantibodies, but the underlying mechanisms by which B cells drive diverse disease presentations in pSS likely extend beyond autoantibody production. Here we outline an expanded role of B cells in disease pathogenesis drawing on examples from animal models of SS, and from other autoimmune diseases that share similar clinical or immunological abnormalities. We focus on recent findings from the detailed analysis of pathogenic B cells in patients with pSS to propose strategies for patient stratification to improve clinical trial outcomes. We conclude that an integrated cellular, molecular and genetic analysis of patients with pSS will reveal the underlying pathogenic mechanisms and guide precision medicine.