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Báo cáo: Review Cells of the synovium in rheumatoid arthritis

Steven K Lundy, Sujata Sarkar, Laura A Tesmer and David A Fox Department of Internal Medicine, Division of Rheumatology and Rheumatic Diseases Core Center, University of Michigan Medical School, 4043 Biomedical Sciences Research Bldg., 109 Zina Pitcher Pl., Ann Arbor, MI 48109-2200, USA Corresponding author: David A Fox, dfox@umich.edu Published: 13 February 2007 This article is online at http://arthritis-research.com/content/9/1/202 © 2007 BioMed Central Ltd Arthritis Research & Therapy 2007, 9:202 (doi:10.1186/ar2107) Abstract Recent findings have substantiated the importance of T lymphocytes to the pathogenesis of rheumatoid arthritis (RA). Here, we review emerging data regarding genetic predisposition, spontaneous animal models of arthritis, and cell-cell interactions that implicate. | Available online http arthritis-research.eom content 9 1 202 Review Cells of the synovium in rheumatoid arthritis T lymphocytes Steven K Lundy Sujata Sarkar Laura A Tesmer and David A Fox Department of Internal Medicine Division of Rheumatology and Rheumatic Diseases Core Center University of Michigan Medical School 4043 Biomedical Sciences Research Bldg. 109 Zina Pitcher Pl. Ann Arbor MI 48109-2200 USA Corresponding author David A Fox dfox@umich.edu Published 13 February 2007 This article is online at http arthritis-research.com content 9 1 202 2007 BioMed Central Ltd Arthritis Research Therapy 2007 9 202 doi 10.1186 ar2107 Abstract Recent findings have substantiated the importance of T lymphocytes to the pathogenesis of rheumatoid arthritis RA . Here we review emerging data regarding genetic predisposition spontaneous animal models of arthritis and cell-cell interactions that implicate T cells as driving synovial inflammation and joint destruction. Information regarding the proinflammatory role of interleukin-17-producing T cells and the functional state of regulatory T cells both in animal models and in patients with RA is also discussed. In light of the overwhelming evidence that disrupted T-cell homeostasis greatly contributes to joint pathology in RA the therapeutic potential of targeting activators of pro-inflammatory T cells or their products is compelling. Introduction Our understanding of how T lymphocytes participate in the pathogenesis of rheumatoid arthritis RA is evolving rapidly with fundamental new insights into basic T-cell biology and the orchestration and regulation of immune responses. The simplistic notion of RA as a homogeneous clonally driven T cell-mediated autoimmune disease is outdated as is the notion that the large numbers of T cells in RA synovium may be irrelevant bystanders. What is replacing these polarized hypotheses is a more integrated view of T cells as a central component of organ-focused immune-mediated pathology capable of .