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Functional variants of interleukin-23 receptor gene confer risk for rheumatoid arthritis but not for systemic sclerosis
  1. Bernadett Faragó (bernadett.farago{at}aok.pte.hu)
  1. University of Pécs, Hungary
    1. Lili Magyari (lili.magyari{at}aok.pte.hu)
    1. University of Pécs, Hungary
      1. Enikõ Sáfrány (eniko.safrany{at}aok.pte.hu)
      1. University of Pécs, Hungary
        1. Veronika Csöngei (veronika.csongei{at}aok.pte.hu)
        1. University of Pécs, Hungary
          1. Luca Járomi (luca.jaromi{at}aok.pte.hu)
          1. University of Pécs, Hungary
            1. Katalin Horvatovich (katalin.z.horvatovich{at}aok.pte.hu)
            1. University of Pécs, Hungary
              1. Csilla Sipeky (csilla.sipeky{at}aok.pte.hu)
              1. University of Pécs, Hungary
                1. Anita Maász (anita.maasz{at}aok.pte.hu)
                1. University of Pécs, Hungary
                  1. Judit Radics (judit.radics{at}aok.pte.hu)
                  1. University of Pécs, Hungary
                    1. Ágnes Gyetvai
                    1. University of Debrecen, Hungary
                      1. Zoltán Szekanecz
                      1. University of Debrecen, Hungary
                        1. László Czirják (laszlo.czirjak{at}aok.pte.hu)
                        1. University of Pécs, Hungary
                          1. Béla Melegh (bela.melegh{at}aok.pte.hu)
                          1. University of Pécs, Hungary

                            Abstract

                            Objectives: Recently, 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 some other autoimmune diseases, including the rheumatoid arthritis (RA) and systemic sclerosis (SSc), we hypothesized, that IL-23R can 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 has 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 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 besides Crohn’s disease some allelic variants or haplogroups of IL-23R represent independent risk factor also for rheumatoid arthritis, but not for scleroderma.

                            • Crohn's disease
                            • interleukin-23 receptor
                            • rheumatoid arthritis
                            • systemic sclerosis

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