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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: Antigen receptor signaling in the rheumatic diseases. | Available online http arthritis-research.eom content 11 1 202 Review Antigen receptor signaling in the rheumatic diseases Julie Zikherman and Arthur Weiss Division of Rheumatology Rosalind Russell Medical Research Center for Arthritis Department of Medicine Howard Hughes Medical Institute University of California San Francisco 513 Parnassus Avenue San Francisco CA 94143 USA Corresponding author Arthur Weiss aweiss@medicine.ucsf.edu Published 30 January 2009 This article is online at http arthritis-research.com content 11 1 202 2009 BioMed Central Ltd Arthritis Research Therapy 2009 11 202 doi 10.1186 ar2528 Abstract Antigen receptor signaling in lymphocytes has been clearly implicated in the pathogenesis of the rheumatic diseases. Here we review evidence from mouse models in which B-cell and T-cell signaling machinery is perturbed as well as data from functional studies of primary human lymphocytes and recent advances in human genetics. B-cell receptor hyper-responsiveness is identified as a nearly universal characteristic of systemic lupus erythematosus in mice and humans. Impaired and enhanced T-cell receptor signaling are both associated with distinct inflammatory diseases in mice. Mechanisms by which these pathways contribute to disease in mouse models and patients are under active investigation. Introduction The classic concept of autoimmune disease rests upon the notion that the adaptive immune system generates inappropriate antigen-specific responses to self epitopes which in turn drive disease. Indeed the presence of autoantibodies is one of the most characteristic features of the rheumatic diseases. Since the canonical definition of the adaptive immune response relates to the ability of somatic recombination to produce an enormous range of antigen receptors on lymphocytes it follows that antigen receptor signal transduction ought to play a role in autoimmune diseases. The T-cell antigen receptor TCR -beta chain was cloned in 1983 and the subsequent decade
