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: Pro-apoptotic Bid is required for the resolution of the effector phase of inflammatory arthritis. | Available online http content 9 3 R49 Research article Pro-apoptotic Bid is required for the resolution of the effector phase of inflammatory arthritis John C Scatizzi1 Jack Hutcheson1 Emily Bickel1 G Kenneth Haines III2 and Harris Perlman1 2 1Saint Louis University School of Medicine Department of Molecular Microbiology and Immunology Saint Louis MO 63104 USA 2Yale University School of Medicine Department of Pathology New Haven CT 06510 USA Corresponding author Harris Perlman perlmanh@ Received 12 Feb 2007 Revisions requested 16 Mar 2007 Revisions received 10 Apr 2007 Accepted 17 May 2007 Published 17 May 2007 Arthritis Research Therapy 2007 9 R49 doi ar2204 This article is online at http content 9 3 R49 2007 Scatizzi 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 Rheumatoid arthritis is an autoimmune disease characterized by hyperplasia of the synovial lining and destruction of cartilage and bone. Recent studies have suggested that a lack of apoptosis contributes to the hyperplasia of the synovial lining and to the failure in eliminating autoreactive cells. Mice lacking Fas or Bim two pro-apoptotic proteins that mediate the extrinsic and intrinsic death cascades respectively develop enhanced K BxN serum transfer-induced arthritis. Since the pro-apoptotic protein Bid functions as an intermediate between the extrinsic and intrinsic apoptotic pathways we examined the role that it plays in inflammatory arthritis. Mice deficient in Bid Bid- - show a delay in the resolution of K BxN serum transfer-induced arthritis. Bid- - mice display increased inflammation bone destruction and pannus formation compared to wild-type mice. Furthermore Bid-
