Báo cáo y học: "Human rheumatoid arthritis tissue production of IL-17A drives matrix and cartilage degradation: synergy with tumour necrosis factor-α, Oncostatin M and response to biologic therapies"

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: Human rheumatoid arthritis tissue production of IL-17A drives matrix and cartilage degradation: synergy with tumour necrosis factor-α, Oncostatin M and response to biologic therapies. | Available online http content 11 4 R113 Research article Human rheumatoid arthritis tissue production of IL-17A drives matrix and cartilage degradation synergy with tumour necrosis factor-a Oncostatin M and response to biologic therapies Ellen M Moran Ronan Mullan Jennifer McCormick Mary Connolly Owen Sullivan Oliver FitzGerald Barry Bresnihan Douglas J Veale and Ursula Fearon Department of Rheumatology St. Vincent s University Hospital Dublin Academic Healthcare and The Conway Institute of Biomolecular and Biomedical Research Elm Park Dublin 4 Ireland Corresponding author Ursula Fearon Received 24 Apr 2009 Revisions requested 1 Jun 2009 Revisions received 20 Jul 2009 Accepted 23 Jul 2009 Published 23 Jul 2009 Arthritis Research Therapy 2009 11 R113 doi 86 ar2772 This article is online at http content 11 4 R113 2009 Moran et al. licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License http licenses by which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Open Access Abstract Introduction The aim of this study was to examine IL-17A in patients following anti-TNF-a therapy and the effect of IL-17A on matrix turnover and cartilage degradation. Methods IL-17A expression was examined by ELISA and immunohistology in the rheumatoid arthritis RA joints. RA whole synovial tissue explant RA ST primary synovial fibroblasts RASFC human cartilage and chondrocyte cultures were stimulated with IL-17A - TNF-a and Oncostatin M OSM . Matrix metalloproteinase MMP and tissue inhibitor TIMP-1 were assessed by ELISA and zymography. Cartilage proteoglycan release was assessed histologically by Safranin-O staining. Clinical parameters IL-17A MMP TIMP were assessed in patients pre post biologic therapy. Results IL-17A levels were higher in RA vs .

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