Journal
IMMUNOLOGICAL REVIEWS
Volume 223, Issue -, Pages 284-299Publisher
WILEY
DOI: 10.1111/j.1600-065X.2008.00646.x
Keywords
autoantibodies; autoimmunity; B lymphocytes; immunotherapy; CD20
Categories
Funding
- NCI NIH HHS [CA105001, CA96547, R01 CA105001, R01 CA096547] Funding Source: Medline
- NIAID NIH HHS [AI56363, U19 AI056363] Funding Source: Medline
- NATIONAL CANCER INSTITUTE [R01CA096547, R01CA105001] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [U19AI056363] Funding Source: NIH RePORTER
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Autoimmunity results from abnormal B- and T-cell recognition of self-antigens, which leads to autoantibody production in many cases. Autoantibodies produced by B-cell-derived plasma cells provide diagnostic markers for autoimmunity but also contribute significantly to disease pathogenesis. As discussed in this review, the therapeutic benefit of depleting B cells in mice and humans has refocused attention on B cells and their role in autoimmunity beyond autoantibody production. B cells specifically serve as cellular adjuvants for CD4(+) T-cell activation, while regulatory B cells, including those that produce interleukin-10 (B10 cells), function as negative regulators of inflammatory immune responses. The emerging picture is that B cells, autoantibodies, and T cells are all important components of abnormal immune responses that lead to tissue pathology unique to each autoimmune disease, with their relative contributions changing during disease progression. Autoimmune diseases where B-cell functions are closely correlated with disease activity include systemic lupus erythematosus, rheumatoid arthritis, scleroderma, type 1 diabetes, and multiple sclerosis. Understanding the overlapping roles of B cells as mediators of autoimmune disease will facilitate the development of more precisely directed therapies and combination therapies with broader clinical efficacy than current depletion strategies that remove all B cells.
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