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: Lessons from animal models of arthritis over the past decade. | Available online http content 11 5 250 Review Lessons from animal models of arthritis over the past decade Wim B van den Berg Rheumatology Research and Advanced Therapeutics Radboud University Nijmegen Medical Center 6525 GA Nijmegen The Netherlands Corresponding author Wim B van den Berg Published 14 October 2009 This article is online at http content 11 5 250 2009 BioMed Central Ltd Arthritis Research Therapy 2009 11 250 doi ar2803 Abstract This review summarizes the major developments in animal models of arthritis in the past decade. It focuses on novel transgenic models addresses the involvement of cytokines and discusses novel findings in cartilage and bone erosion. It is clear that interest has been raised in the direct arthritogenic role of autoantibodies apart from T cell involvement and their interaction with cells through Fcgamma receptors. In addition a role for IL-6 and IL-17 and Th 17 cells seems apparent in most T cell-driven arthritis models with environmental triggering through Toll-like receptors contributing to this process. Further insights into enzymes involved in cartilage proteoglycan loss in arthritis as well as mediators regulating bone erosion and bone apposition have been gained. Introduction Animal models have contributed to the understanding of basic mechanisms of joint disease. There is marked diversity among the numerous models and arthritis has been induced by various stimuli. These include the generation of autoimmunity to cartilage components nonspecific skewing of autoimmunity with adjuvants and triggering with exogenous agents such as bacteria and viruses. More recently focused transgenic manipulation has added novel variants Table 1 . The wide variety of agents that can induce experimental arthritis with histopathological features close to those of human arthritides suggests that disparate etiological pathways may exist in rheumatoid arthritis RA . .
