Background
Autoantibodies directed against citrullinated proteins (e.g. anti-CCP) can be detected in rheumatoid arthritis (RA) patients with very high specificity. The antibodies are present already years before the first clinical symptoms and their presence predicts the development of erosive disease. Citrullinated proteins, the target of anti-CCP antibodies, are formed by post-translational deimination of arginine residues, catalyzed by peptidylarginine deiminase enzymes (PADs). PAD enzymes are expressed by cells present in the inflamed joints of RA patients. These data are the basis of our hypothesis that protein citrullination by PAD is intimately involved in the development of RA.