Thirty years ago, B cells were considered a significant contributing factor in the pathophysiology of rheumatoid arthritis (RA) because of the association of the disease with polyclonal B cell activation and the presence of autoantibodies, such as rheumatoid factor (RF), and immune complexes in the joint ( Hirano 2002 ; Zvaifler 1973 ). However, for much of the past 20 years, RA has mainly been considered a T cell-mediated disease ( Hirano 2002 ). Only recently has new evidence rekindled strong interest in B cells and their important role in the pathogenesis of RA ( Silverman et al. 2003 ).
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