RT Journal Article
SR Electronic
T1 The role of B cells in the pathogenesis of rheumatoid arthritis.
JF The Journal of Rheumatology
JO J Rheumatol
FD The Journal of Rheumatology
SP 14
OP 18
VO 73
A1 Brian L Kotzin
YR 2005
UL http://www.jrheum.org/content/73/14.abstract
AB 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.