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| |  Anti-CD20 Therapy Effective Against B-Cell Depletion in Rheumatoid Arthritis MALDEN, Mass -- June 3, 2008 -- With the goal of identifying reliable predictors of response or relapse to rituximab, a trio of researchers in Germany focused on the recovery response of different B-cell subsets to repeated B-cell depletion. Their analysis, featured in the June 2008 issue of Arthritis & Rheumatism, reveals the critical role of memory B cells in the compromised immune reaction of rheumatoid arthritis (RA) and the short-term gains of rituximab therapy. Conducted by Petra Roll, MD, and Hans-Peter Tony, MD, University of Wurzburg, Wurzburg, Germany, and Thomas Dorner, MD, University of Berlin, Berlin, Germany, the B-cell investigation began with an open-label trial of 1 cycle of rituximab on 17 RA patients. The participants, 14 women and 3 men, had a median age of 51 years, a median disease duration of 14 years, and a history of failure to respond to disease-modifying antirheumatic drug (DMARD) and/or anti-tumour necrosis factor (TNF)-alpha therapy. Blood samples from all participants were obtained at baseline, on day 15, and at a 3-month follow-up, and analysed for B-cell repopulation. After receiving 1 cycle of rituximab, 12 of the 17 patients showed a good clinical response with significant improvement. Within the group of 12 responders, 6 patients experienced an early relapse of RA activity. Eleven patients were re-treated and again achieved a good clinical response. After the second cycle of rituximab, the pattern of B-cell reconstitution was repeated. The number of B cells was still reduced at the time of second depletion but recovered to levels similar to those following the first cycle of therapy. This indicates an unimpaired capacity of B-cell regeneration after repeated B-cell depletion. "Patients with lower numbers of IgD memory cells at the beginning of peripheral B-cell repopulation had a much more favourable clinical response," notes Dr. Tony. "Therefore, the extent of memory B-cell repletion seems to be a key factor influencing the pathophysiology of RA." While revealing a potentially important target for rituximab therapy in RA, this study calls for further research into whether patients with a high level of particular memory B cells may benefit from early re-treatment or may even require higher doses of this anti-CD20 antibody.
SOURCE: Wiley-Blackwell Publishing
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