Báo cáo y học: "Anti-tumour necrosis factor therapy and B cells in rheumatoid arthritis"

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: Anti-tumour necrosis factor therapy and B cells in rheumatoid arthritis. | Available online http content 11 5 128 Editorial Anti-tumour necrosis factor therapy and B cells in rheumatoid arthritis Maria J Leandro Centre for Rheumatology University College London Windeyer Building Room 318 46 Cleveland Street London W1T 4JF UK Corresponding author Maria J Leandro Published 6 October 2009 Arthritis Research Therapy 2009 11 128 doi ar2809 This article is online at http content 11 5 128 2009 BioMed Central Ltd See related research by Souto-Carneiro et al. http content 11 3 R84 Abstract The efficacy of B-cell depletion therapy in rheumatoid arthritis RA has led to a renewed interest in B cells and their products and the role they play in the pathogenesis of the disease. Agents blocking tumour necrosis factor TNF are also very effective in the treatment of RA. It has long been known that the use of anti-TNF therapy can be associated with development of anti-nuclear and anti-double-stranded DNA antibodies and more rarely a lupus-like syndrome. Recently studies have been published investigating further possible effects of anti-TNF agents on B cells and whether these could contribute to their effectiveness in RA. Both blocking tumour necrosis factor TNF and depleting B cells are effective therapeutic strategies in rheumatoid arthritis RA . Recently some articles have focused on possible effects of anti-TNF agents on B cells exploring whether this could contribute to the efficacy of these agents in the treatment of RA. In a study published in a recent issue of Arthritis Research Therapy Souto-Carneiro and colleagues 1 described a decrease in circulating pre-switch IgD CD27 memory B cells in patients with RA when compared with normal controls. Patients with longer disease duration had increased frequency of post-switch IgD-CD27 memory B cells when compared with patients with shorter disease duration or normal controls. Treatment with infliximab was .

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