B cell dysfunctionand pathogenicautoantibodyformationare thoughtto be criticalin the pathogenesis of systemic lupus erythematosus (SLE). In this review we will summarize the results of attempts to utilize B cell depletion, based on the use of a chimeric monoclonalantibody(MAb) specific for human CD20, rituximab, for the treatment of patients with SLE.
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