Pro-apoptotic Bid is required for the resolution of the effector phase of inflammatory arthritis 英文参考文献.docVIP

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Pro-apoptotic Bid is required for the resolution of the effector phase of inflammatory arthritis 英文参考文献.doc

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Pro-apoptotic Bid is required for the resolution of the effector phase of inflammatory arthritis 英文参考文献

Available online /content/9/3/R49 Research article Open Access Vol 9 No 3 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:10.1186/ar2204) This article is online at: /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 (/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. 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. Furthermor