[Pathogenic basis of B cell targeted therapy in systemic lupus erythematosus (SLE)]

Recent success of B-cell targeted therapies in rheumatoid arthritis suggests their potential efficacy for other auntoantibody-mediated autoimmune diseases. Currently, multiple agents directed toward different B-cell specific targets are under development. Although the best strategy is yet to be defined, multiple functional inhibitors or cytolitic agents such as anti-CD20 or anti-CD19 are available. According to studies in RA, the most likely mechanism of action of rituximab (anti-CD20) consists of a secondary reduction in local (synovial) or systemic autoantibody producing short-lived plasma cells. According to this data, it is expected that these therapies will be efficacious in SLE, were B-cell enhanced function and autoantibodies play relevant pathogenetic roles. Clinical trials confirm B-cell effects, delayed activity on autoantibody synthesis, and most importantly, the feasibility of these therapies to treat SLE. However, there are no sufficient data confirming their therapeutic value when added to convencional therapy. Although multiple open trials suggest that rituximab might be useful for refractory manifestations of SLE, more controlled trials are needed in order to establish the indications and strategies of its use in SLE.