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Rheumatology Advance Access originally published online on January 10, 2008
Rheumatology 2008 47(4):409-414; doi:10.1093/rheumatology/kem297
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© The Author 2008. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

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MAPKs and their relevance to arthritis and inflammation

T. Thalhamer, M. A. McGrath and M. M. Harnett

Division of Immunology, Infection and Inflammation, Glasgow Biomedical Research Centre, University of Glasgow, UK.

Correspondence to: M. M Harnett, Division of Immunology, Infection and Inflammation, Glasgow Biomedical Research Centre, University of Glasgow, 120 University Place, Glasgow G12 8TA, UK. E-mail: M.Harnett{at}bio.gla.ac.uk T. Thalhamer and M. A. McGrath equally contributed to this work.


  Abstract

Rheumatoid arthritis (RA) is a chronic autoimmune disease in which imbalances in pro- and anti-inflammatory cytokines promote the induction of autoimmunity, inflammation and joint destruction. The importance of inflammatory cytokines in the pathogenesis of RA has been underscored by the success of biologics that act to block the effects of cytokines, such as tumour necrosis factor-{alpha}, interleukin (IL)-1 or IL-6, in treating disease. Mitogen-activated protein kinases (MAPKs) have been implicated as playing key regulatory roles in the production of these pro-inflammatory cytokines and downstream signalling events leading to joint inflammation and destruction. This article reviews the evidence that MAPKs play important roles in the pathogenesis of RA and discusses their therapeutic potential as drug targets.

KEY WORDS: Mitogen-activated protein kinases, Extracellular signal-regulated kinases, C-jun N-terminal kinase, p38 Mitogen-activated protein kinase, Rheumatoid arthritis, Cytokines

Submitted 2 July 2007; revised version accepted 4 October 2007.
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