Báo cáo y học: "Induction of arthritis by high mobility group box chromosomal protein 1 is independent of tumour necrosis factor signalling"

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: Induction of arthritis by high mobility group box chromosomal protein 1 is independent of tumour necrosis factor signalling. | Available online http content 10 3 R72 Research article Induction of arthritis by high mobility group box chromosomal protein 1 is independent of tumour necrosis factor signalling Rille Pullerits1 Ing-Marie Jonsson1 George Kollias2 and Andrej Tarkowski1 Department of Rheumatology and Inflammation Research Sahlgrenska Academy at Goteborg University Guldhedsgatan 10A 41346 Goteborg Sweden institute of Immunology Biomedical Sciences Research Center Alexander Fleming 34 Al. Fleming Street 1 6672 Vari Greece Corresponding author Rille Pullerits Received 18 Mar 2008 Revisions requested 24 Apr 2008 Revisions received 29 May 2008 Accepted 26 Jun 2008 Published 26 Jun 2008 Arthritis Research Therapy 2008 10 R72 doi ar2445 This article is online at http content 10 3 R72 2008 Pullerits 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 TNFa and high mobility group box chromosomal protein 1 HMGB1 are two potent proinflammatory cytokines implicated as important mediators of arthritis. Increased levels of these cytokines are found in the joints of rheumatoid arthritis patients and the cytokines trigger arthritis when applied into the joints of naive mice. HMGB1 is actively released from immune cells in response to TNFa once released HMGB1 in turn induces production of several proinflammatory cytokines -including IL-6 and TNFa - by macrophages. Whether HMGB1-induced arthritis is mediated via the TNFa pathway however is unknown. The purpose of the present study was to investigate whether the arthritis-inducing effect of HMGB1 is dependent on TNFa expression in vivo and to assess whether TNFa deficiency affects a .

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