For some time, autoimmune diseases have been considered to be mediated essentially by T cells. Of late, emerging data suggest that B cells play an important role in these diseases than previously thought. While it has long been known that levels of autoantibodies such those directed to the thyroid stimulating hormone receptor that correlate with disease severity and progression in Graves disease, and those directed to double-stranded DNA that are often elevated in lupus disease, it is becoming appreciated that B cells play more than one role in these diseases (12). Not only are they the precursors of antibody-secreting plasma cells, but they also act as remarkably effective antigen-presenting cells, suggesting that they may play a potential role in autoimmunity via abnormal autoantigen presentation. B cells can also secrete cytokines, such as TNFa, that exacerbate the autoimmune and inflammatory responses. In addition, autoreactive B cells express ligands that bind costimulatory receptors on T cells. Along with presentation of self-derived peptides on cell surface major histocompatibility complex class II molecules, this can drive activation of autoreactive T cells. Therefore, targeting B cells may prove to be an effective avenue for the development of novel therapies for systemic autoimmune diseases.
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