tailieunhanh - Báo cáo y học: "Rituximab treatment in rheumatoid arthritis: how does it work"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học General Psychiatry cung cấp cho các bạn kiến thức về ngành y đề tài: Rituximab treatment in rheumatoid arthritis: how does it work? | Available online http content 11 6 134 Editorial Rituximab treatment in rheumatoid arthritis how does it work Maria JH Boumans and Paul P Tak Division of Clinical Immunology and Rheumatology Academic Medical Center University of Amsterdam 1100 DE Amsterdam the Netherlands Corresponding author Paul P Tak Published 24 November 2009 Arthritis Research Therapy 2009 11 134 doi ar2852 This article is online at http content 11 6 134 2009 BioMed Central Ltd See related research by Nakou et al. http content 11 4 R131 Abstract Treatment with the chimerical monoclonal antibody rituximab results in CD20-directed B cell depletion. Although this depletion is almost complete in the peripheral blood of nearly all patients with rheumatoid arthritis a proportion of patients does not exhibit a clinical response. The paper by Nakou and colleagues suggests that a decrease in CD19 CD27 memory B cells in both peripheral blood and bone marrow precedes the clinical response to rituximab. This finding adds to the emerging evidence that lack of response to rituximab is associated with persistence of B lineage cells in specific body compartments. In a recent issue of Arthritis Research Therapy Nakou and colleagues 1 present an interesting study of the effects of rituximab treatment on B cell subsets in both peripheral blood and bone marrow of patients with rheumatoid arthritis RA . In 2001 Edwards and Cambridge 2 successfully performed the first pilot trial evaluating B cell depletive therapy in five patients with RA. The beneficial effect of treatment with the B cell depleting chimerical antibody rituximab was confirmed in various placebo-controlled clinical trials and approval followed in 2006 in both the EU and US. The critical role of B cells in the pathogenesis of RA had previously been suggested by the association with autoantibodies rheumatoid factor and anti-citrullinated protein antibodies