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Functional variants of interleukin-23 receptor gene confer risk for rheumatoid arthritis but not for systemic sclerosis
  1. B Faragó1,
  2. L Magyari1,
  3. E Sáfrány1,
  4. V Csöngei1,
  5. L Járomi1,
  6. K Horvatovich1,
  7. C Sipeky1,
  8. A Maász1,
  9. J Radics2,
  10. Á Gyetvai3,
  11. Z Szekanecz4,
  12. L Czirják2,
  13. B Melegh1
  1. 1
    Department of Medical Genetics and Child Development, University of Pécs, Pécs, Hungary
  2. 2
    Department of Immunology and Rheumatology, University of Pécs, Pécs, Hungary
  3. 3
    Laboratory of Immunology, 3rd Department of Internal Medicine, University of Debrecen Medical and Health Science Center, Debrecen, Hungary
  4. 4
    Division of Rheumatology, 3rd Department of Internal Medicine, University of Debrecen Medical and Health Science Center, Debrecen, Hungary
  1. Dr B Melegh, Department of Medical Genetics and Child Development, University of Pécs, H-7624 Pécs, Szigeti út 12, Hungary; Bela.Melegh{at}aok.pte.hu

Abstract

Objectives: Recently, an association was found between Crohn’s disease and the interleukin-23 receptor (IL-23R) gene. Since the IL-23/IL-17 pathway is known to associate with other autoimmune diseases, including rheumatoid arthritis (RA) and systemic sclerosis (SSc), we hypothesised that IL-23R could be a shared susceptibility gene.

Methods: Groups of patients with rheumatoid arthritis (n = 412), systemic sclerosis (n = 224), Crohn’s disease (n = 190) and healthy controls (n = 220) were genotyped for rs10889677 (exon-3’UTR C2370A), rs2201841, and rs1884444 variants; the first two have been shown to confer risk for Crohn’s disease.

Results: We observed an increased prevalence of the homozygous rs10889677 AA and homozygous rs2201841 CC genotypes both in the Crohn’s disease and in the RA groups as compared to the controls (12.1%, 11.9% vs 5.91%, p<0.05; and 13.2%, 13.1% vs 5.91%, p<0.05), but not in the SSc patients. Logistic regression analysis revealed that bearing these alleles represent risk for the development of rheumatoid arthritis (χ2 = 5.58, p = 0.018, OR = 2.15, 95% CI 1.14–4.06 for rs10889677; and χ2 = 7.45, p = 0.006, OR = 2.40, 95% CI 1.28–4.51 for rs2201841). The rs1884444 allele, which has been previously reported as neutral for development of Crohn’s disease, was also found neutral for all studied groups in the present study.

Conclusions: The data reported here provide direct evidence that some allelic variants or haplogroups of IL-23R represent independent risk factors for rheumatoid arthritis as well as Crohn’s disease, but not for scleroderma.

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Footnotes

  • Funding: This work was supported from the grants of Hungarian Scientific Research Foundation OTKA T49589 and OTKA T43017, and from the grant of the Hungarian Ministry of Health ETT 497/2006.

  • Competing interests: None declared

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