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How does B cell depletion therapy work, and how can it be improved?
  1. E A Clark1,
  2. J A Ledbetter2
  1. 1Department of Immunology and National Primate Research Center, University of Washington, Seattle, WA, USA
  2. 2Trubion Pharmaceuticals, 2401 4th Avenue, Suite 1050, Seattle WA 98121, USA
  1. Correspondence to:
    E A Clark
    Department of Immunology and National Primate Research Center, Box 357330, University of Washington, Seattle WA 98195, USA;


The past few years have seen a surge of interest in B cell depletion therapy for patients with rheumatoid arthritis. This paper outlines the possible mechanism(s) by which B cell depletion therapy works. It is likely there is more than one mechanism and the relative importance of each mechanism depends on the target cell. These include CD20-induced apoptosis, complement dependent cytotoxicity, antibody dependent cell-mediated cytotoxicity, and selective targeting and depletion of B cell subsets. The implications of these mechanisms in the further improvement of B cell depletion therapy in rheumatoid arthritis and other autoimmune diseases are discussed.

  • ADCC, antibody dependent cell-mediated cytotoxicity
  • APC, antigen presenting cell
  • CDC, complement dependent cytotoxicity
  • CLL, chronic lymphocytic leukaemia
  • mAb, monoclonal antibody
  • NHL, non-Hodgkin’s lymphoma
  • RA, rheumatoid arthritis
  • B cell depletion therapy
  • CD20
  • rheumatoid arthritis

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  • This work was supported in part by NIH grant RR00166.

  • Competing interests: none declared