When B cells break bad: development of pathogenic B cells in Sjögren’s syndrome

J. H. Reed*, G. M. Verstappen, M. Rischmueller, V. L. Bryant

*Corresponding author for this work

    Research output: Contribution to journalReview articlepeer-review

    1 Citation (Scopus)

    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.

    Original languageEnglish
    Pages (from-to)S271-S282
    Number of pages12
    JournalClinical and Experimental Rheumatology
    Volume38
    Issue number4 Supp. 126
    Publication statusPublished - 23-Oct-2020

    Keywords

    • autoimmunity
    • Sjogren's syndrome
    • B cells
    • precision medicine
    • SYSTEMIC-LUPUS-ERYTHEMATOSUS
    • GENOME-WIDE ASSOCIATION
    • RITUXIMAB TREATMENT
    • RHEUMATOID-FACTOR
    • CARDIAC MANIFESTATIONS
    • DISEASE-ACTIVITY
    • SALIVARY-GLANDS
    • DOUBLE-BLIND
    • BETA(2)-GLYCOPROTEIN I
    • AUTOANTIBODY RESPONSE
    • Autoimmunity
    • Precision medicine
    • Sjögren’s syndrome

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