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Targeting B Cells in SLE: The Experience with Rituximab Treatment (Anti-CD20)

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B cells play a central role in the pathogenesis of SLE. Not only do they make autoantibodies, but they can provide immunoregulatory controls of T cells, dendritic cells, and other B cells, in part through cytokine production. The availability of a chimeric monoclonal antibody that targets B cells has made it possible to treat SLE by B-cell depletion. Rituximab binds to the B-cell specific antigen CD20, and depletes B cells from the peripheral blood and lymphoid tissues. A growing number of anecdotal series and case reports suggest that rituximab may provide clinical benefit in SLE with acceptable toxicity, although the variability in responses of individual patients is not yet fully understood. Two large ongoing randomized controlled trials will determine the efficacy of rituximab in SLE, both renal and extra-renal, and will inform us better about the biology of the B cell in this disease and the effects of B-cell depletion.

Keywords: B cells; CD20; SLE; chimeric monoclonal antibody; rituximab

Document Type: Research Article


Affiliations: Division of Rheumatology, Department of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.

Publication date: December 1, 2006

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  • This journal is devoted to timely reviews of experimental and clinical studies in the field of endocrine, metabolic, and immune disorders. Specific emphasis is placed on humoral and cellular targets for natural, synthetic, and genetically engineered drugs that enhance or impair endocrine, metabolic, and immune parameters and functions. Topics related to the neuroendocrine-immune axis are given special emphasis in view of the growing interest in stress-related, inflammatory, autoimmune, and degenerative disorders.

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