

Author: Leandro Maria J Cambridge Geraldine Edwards Jonathan CW
Publisher: Future Medicine
ISSN: 1746-0816
Source: Future Rheumatology, Vol.1, Iss.4, 2006-08, pp. : 493-499
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Abstract
B-cell depletion based on rituximab has now been proven to be an effective therapy for seropositive rheumatoid arthritis with a good safety profile. The encouraging results from early, open-label trials have been confirmed in three large, controlled trials. A license for use in patients that have failed antitumor necrosis factor-α agents has been obtained in the USA and is imminent in several other countries. Despite this welcome progress, experience suggests that all patients who respond to B-cell depletion eventually show clinical relapse. Possible mechanisms of relapse include incomplete depletion of pathogenic B cell clones, persistence of long-lived plasma cells producing pathogenic autoantibodies, or persistence of other kinds of cells, such as autoreactive T cells carrying ‘disease memory’. A better understanding of why patients relapse may allow us to optimize B-cell depletion protocols based on rituximab and/or other agents and contribute to the development of B-cell-targeted therapies, with the ultimate goal of long-term remission.
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