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Rheumatoid arthritis: an antigenic chameleon
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  1. Eugen Feist1,
  2. Guenter Steiner2
  1. 1Department of Rheumatology and Clinical Immunology, Charite University Hospital, Berlin, Germany
  2. 2Department of Rheumatology, Clinic for Internal Medicine III, Medical University Vienna, Vienna, Austria
  1. Correspondence to Dr Eugen Feist, Department of Rheumatology and Clinical Immunology, Charite University Hospital, Charitéplatz 1, Berlin 10117, Germany; eugen.feist{at}charite.de

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Nowadays, rheumatologists and immunologists have to be absorptive like a sponge—from a breathtaking progress in the basic research field to emerging approaches in diagnosis and treatment of complex disorders like rheumatoid arthritis (RA), there is always exciting and sometimes unexpected news to digest.

For those who are particularly interested in the autoimmune response in RA, we have to realise that we are engaged with a true chameleon. Since the discovery more than 15 years ago of humoral autoimmune reactivities to epitopes containing the unusual amino acid citrulline,1 many new autoimmune targets have been discovered and, even more important, also different post-translational modifications to push their antigenic properties. Meanwhile the best understood process represents enzymatic deimination of peptide—or protein-bound arginine to citrulline. In genetically prone individuals, this activity creates highly specific recognition motives for auto-antibodies (anti-citrullinated protein/peptide antibodies, ACPAs), which serve as excellent diagnostic markers, especially in the early phases of disease. Since citrullination, as a physiological process, is also triggered by …

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