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: Increased interleukin-17 production via a phosphoinositide 3-kinase/Akt and nuclear factor κB-dependent pathway in patients with rheumatoid arthritis. | Available online http content 7 1 R139 Research article Increased interleukin-17 production via a phosphoinositide 3-kinase Akt and nuclear factor KB-dependent pathway in patients with rheumatoid arthritis Kyoung-Woon Kim Mi-La Cho Mi-Kyung Park Chong-Hyeon Yoon Sung-Hwan Park Sang-Heon Lee and Ho-Youn Kim Open Access Department of Medicine Division of Rheumatology The Center for Rheumatic Diseases and The Rheumatism Research Center RhRC Catholic Research Institutes of Medical Sciences Catholic University of Korea Seoul Korea Contributed equally Corresponding author Sang-Heon Lee shlee@ Received 27 Apr 2004 Revisions requested 19 May 2004 Revisions received 18 Oct 2004 Accepted 3 Nov 2004 Published 29 Nov 2004 Arthritis Res Ther 2005 7 R139-R148 DOI ar1470 2004 Kim 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. Abstract Inflammatory mediators have been recognized as being important in the pathogenesis of rheumatoid arthritis RA . Interleukin IL -17 is an important regulator of immune and inflammatory responses including the induction of proinflammatory cytokines and osteoclastic bone resorption. Evidence for the expression and proinflammatory activity of IL-17 has been demonstrated in RA synovium and in animal models of RA. Although some cytokines IL-15 and IL-23 have been reported to regulate IL-17 production the intracellular signaling pathways that regulate IL-17 production remain unknown. In the present study we investigated the role of the phosphoinositide 3-kinase PI3K Akt pathway in the regulation of IL-17 production in RA. Peripheral blood mononuclear cells PBMC from patients with RA n 24 were separated then stimulated with various agents including anti-CD3 .
