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Rheumatology Advance Access originally published online on September 13, 2005
Rheumatology 2006 45(1):26-30; 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

REVIEW

Fas (CD95)-related apoptosis and rheumatoid arthritis

S. L. Peng

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

Correspondence to: S. L. Peng, Inflammation, Autoimmunity and Transplantation Research, Roche Palo Alto, 3431 Hillview Ave, MailStop R7-101, Palo Alto, CA 94025, USA. E-mail: stanford.peng{at}roche.com

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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