The realization of the central role of T cells and cytokines in the disease has led to a remarkable advance in treatment, in which specific molecules have been targeted on the basis of scientific understanding. Chief among these new therapies are antagonists against TNF, which have transformed the course of the disease in many patients from one of progressive and inexorable joint destruction to one of smoldering but manageable chronic inflammation. An IL-1 antagonist and an antibody against the IL-6 receptor are approved treatments, as is a fusion protein of the extracellular domain of CTLA-4 and the Fc portion of IgG, which binds to B7 molecules and blocks B7:CD28 interactions. Antibodies that block IL-17 are in clinical trials. The B cell-depleting anti-CD20 antibody is of benefit in some patients. The beneficial effect of B cell depletion does not seem to be attributable entirely to reduced production of autoantibodies, suggesting that B cells may play other roles in the disease, such as presenting antigens to pathogenic T cells.
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