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Rheumatology Advance Access published online on September 13, 2005
Rheumatology, doi:10.1093/rheumatology/kei113
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© The Author 2005. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
Received July 8, 2005
Accepted August 9, 2005

Review Article

Fas (CD95)-related apoptosis and rheumatoid arthritis

S. L. Peng 1*

1 Inflammation, Autoimmunity and Transplantation Research, Roche Palo Alto, Palo Alto, CA, USA

* To whom correspondence should be addressed.
S. L. Peng, E-mail: stanford.peng{at}roche.com


  Abstract

Abnormal proliferation and/or persistence of synoviocytes and inflammatory cells has long been described in inflammatory arthritis conditions, but only relatively recently has substantial attention been drawn to the relevance of abnormal apoptotic processes in disease pathogenesis and treatment. This review summarizes a current understanding of the Fas (CD95)-Fas ligand (CD178) apoptotic system, which has most predominantly been examined in rheumatoid arthritis. There, synovial inflammation is often characterized by a unique resistance to Fas-related apoptosis, and agonistic therapeutic interventions upon Fas have consistently been found beneficial in both animal and human disease models. Therefore, modulation of the Fas pathway will hopefully be of both pathogenic and therapeutic interest in the study of inflammatory arthritis conditions in general.


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