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Arthritis Research & Therapy
Published in: Arthritis Research & Therapy 3/2007

Open Access 01-06-2007 | Research article

Pro-apoptotic Bid is required for the resolution of the effector phase of inflammatory arthritis

Authors: John C Scatizzi, Jack Hutcheson, Emily Bickel, G aKenneth Haines III, Harris Perlman

Published in: Arthritis Research & Therapy | Issue 3/2007

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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-/- mice have elevated levels of CXC chemokine and IL-1β in serum, which are associated with more inflammatory cells throughout the arthritic joint. In addition, there are fewer apoptotic cells in the synovium of Bid-/- compared to Wt mice. These data suggest that extrinsic and intrinsic apoptotic pathways cooperate through Bid to limit development of inflammatory arthritis.
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Metadata
Title
Pro-apoptotic Bid is required for the resolution of the effector phase of inflammatory arthritis
Authors
John C Scatizzi
Jack Hutcheson
Emily Bickel
G aKenneth Haines III
Harris Perlman
Publication date
01-06-2007
Publisher
BioMed Central
Published in
Arthritis Research & Therapy / Issue 3/2007
Electronic ISSN: 1478-6362
DOI
https://doi.org/10.1186/ar2204

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