Title | B-lymphocyte contributions to human autoimmune disease. |
Publication Type | Journal Article |
Year of Publication | 2008 |
Authors | Yanaba K, Bouaziz J-D, Matsushita T, Magro CM, E St Clair W, Tedder TF |
Journal | Immunol Rev |
Volume | 223 |
Pagination | 284-99 |
Date Published | 2008 Jun |
ISSN | 1600-065X |
Keywords | Animals, Antibodies, Monoclonal, Antibodies, Monoclonal, Murine-Derived, Antigen Presentation, Autoimmune Diseases, B-Lymphocytes, CD4-Positive T-Lymphocytes, Humans, Immunologic Memory, Immunotherapy, Interleukin-10, Lymphocyte Activation, Lymphocyte Depletion, Mice, Rituximab |
Abstract | SUMMARY: 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. |
DOI | 10.1111/j.1600-065X.2008.00646.x |
Alternate Journal | Immunol Rev |
PubMed ID | 18613843 |
Grant List | AI56363 / AI / NIAID NIH HHS / United States CA96547 / CA / NCI NIH HHS / United States CA105001 / CA / NCI NIH HHS / United States |
Related Faculty:
Cynthia M. Magro, M.D.