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.
Highlights
Citrullination is a post-translational modification catalysed by peptidylarginine deiminase and is a common feature of inflammation
They found by immunohistochemistry that intracellular citrullination, as determined by F95 antibody staining, as well as peptidylarginine deiminase (PAD) expression were correlated with measures of synovial inflammation
*Correspondence: benjamin.fisher@imperial.ac.uk 1Department of Rheumatology, Imperial College Healthcare NHS Trust, Charing Cross Hospital, London W6 8RF, UK Full list of author information is available at the end of the article
Summary
Citrullination is a post-translational modification catalysed by peptidylarginine deiminase and is a common feature of inflammation. Makrygiannakis and colleagues study the effect on synovial citrullination of treatment with two commonly used drugs in the treatment of rheumatoid arthritis (RA) [1]. They found by immunohistochemistry that intracellular citrullination, as determined by F95 antibody staining, as well as peptidylarginine deiminase (PAD) expression were correlated with measures of synovial inflammation.
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