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Highly Accessed Editorial

Inhibiting citrullination in rheumatoid arthritis: taking fuel from the fire

Benjamin AC Fisher1* and Patrick J Venables2

Author Affiliations

1 Department of Rheumatology, Imperial College Healthcare NHS Trust, Charing Cross Hospital, London W6 8RF, UK

2 Kennedy Institute of Rheumatology, University of Oxford, 65 Aspenlea Road, London W6 8LH, UK

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Arthritis Research & Therapy 2012, 14:108  doi:10.1186/ar3740


See related research by Makrygiannakis et al., http://arthritis-research.com/content/14/1/R20

Published: 29 February 2012

Abstract

Citrullination is a post-translational modification catalysed by peptidylarginine deiminase and is a common feature of inflammation. The presence of anti-citrullinated protein/peptide antibodies (ACPA), however, is unique to rheumatoid arthritis. Several lines of evidence suggest that ACPA are important in the pathogenesis of rheumatoid arthritis. A popular hypothesis for this pathogenesis is a two-hit model. The first hit gives rise to ACPA, and the second hit, an unrelated episode of synovial inflammation accompanied by citrullination, is perpetuated by the pre-existing antibodies. This model suggests that reducing citrullination might ameliorate disease. Recent findings indicate that citrullination closely correlates with inflammation, and that glucocorticoids decrease peptidylarginine deiminase expression independent of their other anti-inflammatory effects.