Current Rheumatology Reports

, Volume 5, Issue 5, pp 350–356

B cell depletion therapy in systemic lupus erythematosus

Authors

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

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

Abstract

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.

Download to read the full article text

Copyright information

© Current Science Inc. 2003