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, featured in the June 2008 issue of Arthritis & Rheumatism (www.interscience.wiley.com/journal/arthritis), reveals the critical role of memory B cells in the compromised immune reaction of RA and the short-term gains of rituximab therapy.
Conducted by Petra Roll, M.D., and Hans-Peter Tony, M.D., at the University of Wrzburg and Thomas Drner, M.D., an affiliate of the University of Berlin, the B cell investigation began with an open-label trial of one 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 DMARD and/or anti-TNFα therapy. 16 of the patients received 2 infusions rituximab, 1,000 milligrams each, 2 weeks apart, and one patient received 4 weekly infusions of rituximab at a dose of 375 mill
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