Targeting CD22 as a strategy for treating systemic autoimmune diseases

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Authors: Thomas Dörner, David M Goldenberg

Published Date November 2007 Volume 2007:3(5) Pages 953 - 959

DOI: http://dx.doi.org/10.2147/TCRM.S

Thomas Dörner¹, David M Goldenberg²

¹Charite University Hospital Berlin and Deutsche Rheumaforschungszentrum, Berlin, Germany; ²Center for Molecular Medicine and Immunology, Belleville, New Jersey, USA

Abstract: B-cells play an important role in the diagnosis and to some extent the pathogenesis of many autoimmune diseases. Specific B-cell directed antibodies are now gaining an increasing role in the management of these diseases. The first antibody target in this regard was CD20, with the development and introduction of rituximab in the management of B-cell malignancies as well as rheumatoid arthritis. A second candidate target is CD22, and the first antagonistic antibody to this B-cell marker is epratuzumab, which appears to function, in contrast to CD20 antibodies, more by modulation of B-cells than by their depletion capacity. Originally developed for the treatment of non-Hodgkin lymphoma, epratuzumab has now been reported to be effective, with a very good safety profile, in two prototype autoimmune diseases, systemic lupus erythematosus and primary Sjögren’s syndrome. As such, this new investigational antibody may provide distinct therapeutic effects and may be complementary to the known effects and role of CD20 antibodies.

Keywords: autoimmune diseases, CD22, B-cells, epratuzumab