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Báo cáo y học: "A proinflammatory role for Fas in joints of mice with collagen-induced 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: A proinflammatory role for Fas in joints of mice with collagen-induced arthritis. | Available online http arthritis-research.eom content 6 5 R404 Research article A proinflammatory role for Fas in joints of mice with collagen-induced arthritis Hoang Tu-Rapp1 André Hammermuller1 Eilhard Mix2 Hans-Jurgen Kreutzer3 Roland Goerlich4 Hansjurgen Kohler1 Horst Nizze3 Hans-Jurgen Thiesen1 and Saleh M Ibrahim1 Department of Immunology University of Rostock Rostock Germany 2Department of Neurology University of Rostock Rostock Germany 3Department of Pathology University of Rostock Rostock Germany 4Institute of Biology VII RWTH Aachen Aachen Germany Corresponding author Hoang Tu-Rapp hoang.tu-rapp@med.uni-rostock.de Received 11 Feb 2004 Revisions requested 3 Mar 2004 Revisions received 30 Apr 2004 Accepted 7 Jun 2004 Published 19 Jul 2004 Arthritis Res Ther 2004 6 R404-R414 DOI 10.1186 ar1 205 2004 Tu-Rapp et al. licensee BioMed Central Ltd. This is an Open Access article verbatim copying and redistribution of this article are permitted in all media for any purpose provided this notice is preserved along with the article s original URL. Open Access Abstract Collagen-induced arthritis CIA is a chronic inflammatory disease bearing all the hallmarks of rheumatoid arthritis e.g. polyarthritis synovitis and subsequent cartilage bone erosions. One feature of the disease contributing to joint damage is synovial hyperplasia. The factors responsible for the hyperplasia are unknown however an imbalance between rates of cell proliferation and cell death apoptosis has been suggested. To evaluate the role of a major pathway of cell death - Fas CD95 FasL - in the pathogenesis of CIA DBA 1J mice with a mutation of the Fas gene Ipr were generated. The susceptibility of the mutant DBA-lpr lpr mice to arthritis induced by collagen type II was evaluated. Contrary to expectations the DBA-lpr lpr mice developed significantly milder disease than the control littermates. The incidence of disease was also significantly lower in the lpr lpr mice than in the controls 40 versus 81 P .