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Rheumatology Advance Access originally published online on May 21, 2008
Rheumatology 2008 47(10):1446-1451; doi:10.1093/rheumatology/ken197
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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

REVIEWS

Fractalkine in rheumatoid arthritis: a review to date

G. Murphy1, N. Caplice2 and M. Molloy1

1Department of Rheumatology, Cork University Hospital and 2Centre for Research in Vascular Biology, University College Cork, Cork, Ireland.

Correspondence to: G. Murphy, Department of Rheumatology, Cork University Hospital, Wilton, Cork, Ireland. E-mail: grainne.murphy{at}ucc.ie


  Abstract

Rheumatoid arthritis (RA) is characterized by the expansion of the synovium, with infiltration of pro-inflammatory cells, neovascularization and an abundance of pro-inflammatory cytokines resulting in tissue destruction and bone erosion. Fractalkine (FKN), a recently described chemokine, possesses chemotactic, angiogenic and adhesive functions that associates it with all of these destructive processes. In this review, we describe the research to date, which implicates FKN and its receptor in the pathogenesis of RA and propose that this molecule may represent a future therapeutic target for RA.

KEY WORDS: Fractalkine, Angiogenesis, Chemotaxis, Rheumatoid

Submitted 7 January 2008; revised version accepted 15 April 2008.
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