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
- rheumatoid arthritis
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This work was supported in part by NIH grant RR00166.
Competing interests: none declared