Functional variants of interleukin-23 receptor gene confer risk for rheumatoid arthritis but not for systemic sclerosis: Table 1

Autor: Ágnes Gyetvai, Katalin Horvatovich, Bernadett Faragó, Lili Magyari, Veronika Csöngei, Judit Radics, Csilla Sipeky, László Czirják, Béla Melegh, Anita Maász, Eniko Safrany, Luca Jaromi, Zoltán Szekanecz
Rok vydání: 2007
Předmět:
Zdroj: Annals of the Rheumatic Diseases. 67:248-250
ISSN: 1468-2060
0003-4967
DOI: 10.1136/ard.2007.072819
Popis: 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 2 = 5.58, p = 0.018, OR = 2.15, 95% CI 1.14–4.06 for rs10889677; and χ 2 = 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.
Databáze: OpenAIRE