B cells play an important role in the pathogenesis of certain lymphomas and leukemias, as well as many autoimmune diseases. Antagonistic B-cell antibodies are thus 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. The first antagonistic antibody to this B-cell marker, epratuzumab, appears to function, in contrast to CD20 antibodies, more by modulation of B cells rather than by their high depletion in circulation. Originally developed for the treatment of non-Hodgkin's lymphoma, epratuzumab has now been found to be effective, with a very good safety profile, in two prototype autoimmune diseases: systemic lupus erythematosus and primary Sjogren's syndrome. Recent studies have demonstrated the activity and safety of epratuzumab in non-Hodgkin's lymphoma patients who have relapsed or are refractive to conventional therapy, including rituximab, and has also shown good activity in follicular and diffuse large B-cell lymphoma in combination with rituximab. As such, this new investigative antibody may have a significant market potential owing to the multitude of diseases and patients who may benefit from a CD22, B-cell antibody immunotherapy that is complementary to the known effects and role of CD20 antibodies, but can usually be administered within I h and depletes approximately 50% of circulating B cells.
