tailieunhanh - Báo cáo y học: "α Paradoxical effects of tumour necrosis factor-α in adjuvant-induced 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: α Paradoxical effects of tumour necrosis factor-α in adjuvant-induced arthritis. | Available online http content 10 3 113 Editorial Paradoxical effects of tumour necrosis factor-a in adjuvant-induced arthritis Richard O Williams Kennedy Institute of Rheumatology Division Imperial College London Aspenlea Road London W6 8LH UK Corresponding author Richard O Williams Published 6 June 2008 Arthritis Research Therapy 2008 10 113 doi ar2430 This article is online at http content 10 3 113 2008 BioMed Central Ltd See related research article by Kim et al. http content 10 2 R38 Abstract Anti-tumour necrosis factor TNF a therapy is highly effective in rheumatoid arthritis and it is surprising therefore that a recent study showed that intraperitoneal administration of recombinant TNFa reduced the severity of adjuvant-induced arthritis and decreased IFNy expression in cultured draining lymph node cells. Furthermore in untreated arthritic rats maximal TNFa expression in draining lymph node cells coincided with spontaneous disease remission suggesting a role for endogenous TNFa in recovery from arthritis. If confirmed in further studies these findings suggest that in addition to its well-established pro-inflammatory properties TNFa may also play a disease-limiting role in this model of rheumatoid arthritis by suppressing effector T cell responses. A recent paper by Kim and colleagues 1 published in this journal reports that intraperitoneal administration of recombinant tumour necrosis factor rTNF a to rats with adjuvant-induced arthritis has a beneficial effect on disease outcome. This is surprising given the efficacy of anti-TNFa therapy in rheumatoid arthritis RA 2 with patients receiving not only immediate clinical benefit but also reduced joint damage in the long-term 3 . How can we reconcile the fact that blockade of endogenous TNFa is beneficial in human RA whereas administration of exogenous rTNFa reduces disease severity in an animal model of