B cells, precursors of autoantibody-secreting cells, have emerged as promising new therapeutic targets in autoimmune diseases, including rheumatoid arthritis (RA). In particular, B cell depletion with the anti-CD20 antibody rituximab seems to work for RA patients resistant to standard disease-modifying antirheumatic drugs (DMARDs) and tumor necrosis factor α (TNFα) blockers. In large trials, about half of these hard-to-treat patients respond to rituximab, achieving at least a 20 percent improvement in disease activity based on the American College of Rheumatology criteria. However, in the majority of responders, the disease relapses over time. After a single treatment with rituximab, complete remission of RA symptoms for longer than a year is very rare.
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 reveals the critical role of memory B cells in the compromised immune reaction of RA and the short-term gains of rituximab therapy.
http://www.sciencedaily.com/releases/2008/06/080602160801.htm
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