tailieunhanh - Báo cáo y học: "High mobility group box-1 protein as a tumor necrosis factor-independent therapeutic target 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: High mobility group box-1 protein as a tumor necrosis factor-independent therapeutic target in rheumatoid arthritis. | Available online http content 10 3 111 Editorial High mobility group box-1 protein as a tumor necrosis factor-independent therapeutic target in rheumatoid arthritis Richard S Goldstein Department of Emergency Medicine and The Feinstein Institute for Medical Research North Shore University Hospital Community Drive Manhasset NY 11030 USA Corresponding author Richard S Goldstein rgoldst2@ Published 2 June 2008 Arthritis Research Therapy 2008 10 111 doi ar2427 This article is online at http content 10 3 111 2008 BioMed Central Ltd See related research article by Sundberg et al. http content 10 2 R33 Abstract Rheumatoid arthritis RA remains a prevalent disease worldwide that causes significant morbidity and mortality despite recent therapeutics. High mobility group box-1 HMGB1 protein originally appreciated as an intranuclear DNA binding protein has been implicated as an integral mediator in the pathogenesis of animal arthritides and RA disease in humans. Our current understanding of HMGB1 has promoted the development of targeting therapies that have improved outcomes in animal models of inflammation. In the previous issue of Arthritis Research Therapy Sundberg and colleagues address for the first time in a prospective cohort study whether HMGB1 expression is dependent upon tumor necrosis factor activity in patients with RA. Introduction Rheumatoid arthritis RA is an autoimmune chronic destructive polyarthropathy that has a worldwide prevalence of to 1 and an incidence of 3 cases per 10 000 persons annually. Over-expression of pro-inflammatory cytokines including tumor necrosis factor TNF and interleukin IL -1 play a critical role in the pathogenesis of RA and is the basis for RA targeting strategies in recent years. In the previous issue of Arthritis Research Therapy Sundberg and colleagues 1 set forth to determine whether anti-TNF therapy influences synovial and extracellular high