Current Rheumatology Reports

, Volume 5, Issue 5, pp 350–356

B cell depletion therapy in systemic lupus erythematosus


  • Jennifer Anolik
    • Department of Medicine: Immunology and RheumatologyUniversity of Rochester School of Medicine
  • Iñaki Sanz
  • R. John Looney

DOI: 10.1007/s11926-003-0020-x

Cite this article as:
Anolik, J., Sanz, I. & Looney, R.J. Curr Rheumatol Rep (2003) 5: 350. doi:10.1007/s11926-003-0020-x


There is a growing body of experimental evidence that B lymphocytes play a central role in the pathogenesis of systemic lupus erythematosus (SLE). B cells are, by definition, the precursors of antibody-secreting cells, and thus are the source of pathogenic autoantibodies. However, recent data indicate that B cells are not merely the passive producers of immunoglobulins, but also play a central role in autoimmunity via nonconventional mechanisms, including autoantigen presentation and modulation of other immune cells. Thus, B lymphocyte depletion has recently emerged as a promising therapeutic approach to the treatment of autoimmune diseases, including SLE. Rituximab is a chimeric mouse-human monoclonal antibody against the B cell-specific antigen CD20, which selectively and profoundly depletes B lymphocytes and has been widely used to treat B cell lymphomas. Recent open-label studies indicate that rituximab is safe and may be efficacious in the treatment of SLE, and continued study with randomized clinical trials is justified.

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© Current Science Inc. 2003