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New rheumatoid arthritis genetic factor and C5 serum level
  1. H Mbarek1,
  2. M Kallel-Sellami2,
  3. Y Zerzri2,
  4. K Dawidowicz1,
  5. K Mejri2,
  6. T Bardin3,
  7. B Prum4,
  8. P Dieudé1,5,
  9. E Petit-Teixeira1,
  10. F Cornélis1,6,7,
  11. S Makni8
  1. 1
    GenHotel, EA3886, Laboratoire de Recherche Européen pour la Polyarthrite Rhumatoïde, Évry, France
  2. 2
    Laboratoire d’Immunologie, Hôpital la Rabta, Tunis, Tunisia
  3. 3
    Département de Rhumatologie, Hôpital Lariboisière, Paris, France
  4. 4
    Laboratoire Statistique & Génome, Évry, France
  5. 5
    Département de Rhumatologie, Hôpital Bichat, Paris, France
  6. 6
    Centre Hospitalier Sud Francilien, Corbeil-Essonnes, France
  7. 7
    Unité de Génétique Clinique, Hôpital Lariboisière, Paris, France
  8. 8
    Laboratoire d’Immunologie, Hôpital la Rabta, Tunis, Tunisia
  1. Correspondence to H Mbarek, GenHotel, EA3886, Laboratoire de Recherche Européen pour la Polyarthrite Rhumatoïde, Université Evry-Val d’Essonne – Université Paris 7, 2 Rue Gaston Crémieux, CP 5727, 91057 Evry Genopole Cedex, France; hamdi{at}polyarthrite.net

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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 …

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