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There is a significant body of evidence suggesting that complement activation plays an important role in the maintenance of the polyarticular chronic synovitis characteristic of rheumatoid arthritis (RA).1 Recently, a novel RA genetic risk factor was described, involving allelic polymorphisms on the chromosome 9, in the intergenic region between complement factor 5 (C5) and tumour necrosis factor receptor-associated factor 1 (TRAF1) genes.2,3,4 The new genetic factor, detected in RA case-control studies for anti-cyclic citrullinated peptide antibodies and/or rheumatoid factor positive (RF+) RA in North American, Swedish and Dutch populations,2,3 was confirmed by linkage in a …
Funding The Association Française des Polyarthritiques, Association Rhumatisme et Travail, the European Union for AutoCure, CMCU (Comité Mixte de Coopération Universitaire Franco-Tunisienne) and La Rabta Hospital, Tunis funded this study.
Competing interests None declared.
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