J Rheumatol Suppl. 2005 Feb;73:14-8; discussion 29-30.

The role of B cells in the pathogenesis of rheumatoid arthritis.

Source

Denver Autoimmunity Center of Excellence, University of Colorado Health Sciences Center, Denver, Colorado, USA. bkotzin@amgen.com

Abstract

The classical paradigm for rheumatoid arthritis (RA) pathogenesis holds that CD4+ T cells mediate joint damage both directly and by driving non-T effector cells to release inflammatory cytokines. By contrast, the new paradigm that is developing centers on an interaction of CD4+ T cells with B cells. Evidence reviewed in this article shows that autoreactive B cells can be driven by the T cells to produce IgG autoantibodies that may be directly involved in joint damage, and B cells are known to be critical in activating CD4+ T cells. As the B cell appears to play an important role in the RA process, it is appropriate to consider how B cell-mediated effects might be reduced or prevented in patients with this disease. As the targeted depletion of B cells with a monoclonal antibody such as rituximab appears to be clinically effective in RA patients, this approach shows great therapeutic potential.

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