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A re-evaluation of three putative functional single nucleotide polymorphisms in rheumatoid arthritis
  1. D Plant1,
  2. A Barton1,
  3. W Thomson1,
  4. X Ke1,
  5. S Eyre1,
  6. A Hinks1,
  7. J Bowes1,
  8. L J Gibbons1,
  9. A G Wilson2,
  10. I Marinou2,
  11. A W Morgan3,
  12. S Steer4,
  13. L J Hocking5,
  14. D M Reid5,
  15. P Wordsworth6,
  16. P Harrison6,
  17. J Worthington1
  1. 1
    arc-Epidemiology Unit, University of Manchester, Manchester, UK
  2. 2
    School of Medicine and Biomedical Sciences, University of Sheffield, Sheffield, UK
  3. 3
    Leeds Institute of Molecular Medicine, St James’s University Hospital, Leeds, UK
  4. 4
    Clinical and Academic Rheumatology, Kings College Hospital NHS Foundation Trust, London, UK
  5. 5
    Division of Applied Medicine, School of Medicine and Dentistry, University of Aberdeen, Aberdeen, UK
  6. 6
    University of Oxford Institute of Musculoskeletal Sciences, Botnar Research Centre, Nuffield Orthopaedic Centre, Oxford, UK
  1. Dr D Plant, arc-Epidemiology Unit, Stopford Building, University of Manchester, Manchester M13 9PT, UK; darren.plant{at}manchester.ac.uk

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In European rheumatoid arthritis (RA) patients, the strongest genetic effects are conferred by the HLA-DRB1 locus1 and the protein tyrosine phosphatase 22 gene (PTPN22).2 A further three susceptibility loci (OLIG3/TNFAIP3, TRAF1/C5 and STAT4) have been confirmed.3 4 All five loci associate with RA in UK patients.5

Functional variants of the Fc receptor-like 3 gene (FCRL3), the solute carrier 22 member 4 gene (SLC22A4) and the major histocompatibility complex, class II, transactivator gene (MHC2TA) associate with RA in some but not all populations.

We have previously investigated polymorphisms in FCRL3, MHC2TA and SLC22A4 in moderately sized UK studies and not detected evidence of association.68 Here we revisit these putative RA …

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