TAILIEUCHUNG - Báo cáo y học: "Cell signalling in macrophages, the principal innate immune effector cells of 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: Cell signalling in macrophages, the principal innate immune effector cells of rheumatoid arthritis. | Available online http content 10 5 216 Review Cell signalling in macrophages the principal innate immune effector cells of rheumatoid arthritis Stefan K Drexler Philip L Kong Jeremy Wales and Brian M Foxwell Kennedy Institute of Rheumatology Division Faculty of Medicine Imperial College of Science Technology and Medicine 65 Aspenlea Road Hammersmith London W6 8LH UK Corresponding author Brian M Foxwell Published 10 October 2008 This article is online at http content 10 5 216 2008 BioMed Central Ltd Arthritis Research Therapy 2008 10 216 doi ar2481 Abstract Rheumatoid arthritis is a multisystemic auto-inflammatory disease affecting up to 1 of the population and leading to the destruction of the joints. Evidence exists for the involvement of the innate as well as the adaptive immune systems in the pathology of the disease. The success of anti-tumour necrosis factor-a indicates the importance of pro-inflammatory mediators produced by innate immune cells in rheumatoid arthritis progression. Therefore considerable efforts have been made in elucidating the signalling pathways leading to the expression of those mediators. This review will concentrate on the role of signalling pathways in innate immune cells in the context of rheumatoid arthritis. Introduction The immune system evolved as a mechanism to protect organisms from infection by pathogenic organisms and other harmful substances. In general the immune system is capable of recognising invading pathogens and their products as well as endogenous danger signals 1 . This recognition results in the initiation of an immune response which will under normal circumstances eliminate the insult without further damage to the host. However it is now well recognised that defects in regulating inflammation can lead to an excessive response to infectious agents such as sepsis or auto-inflammatory diseases such as rheumatoid arthritis RA . In the context

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