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    Rheumatol Int. 2009 May;29(7):781-6. Epub 2008 Nov 26.

    Lack of association between interleukin 23 receptor gene polymorphisms and rheumatoid arthritis susceptibility.

    Park JH, Kim YJ, Park BL, Bae JS, Shin HD, Bae SC.

    Source

    Division of Rheumatology, Department of Internal Medicine, Hanyang University College of Medicine, The Hospital for Rheumatic Diseases, Hanyang University, 17 Haengdang-Dong, Seongdong-Gu, Seoul, 133-792, South Korea.

    Abstract

    The recent discovery of interleukin 23 (IL-23), its receptor, and the underlying signal transduction pathway has improved our understanding of cellular immunity. Several studies suggest that IL-23 is an essential promoter of chronic joint inflammation. In this report, we assess the possible association of interleukin 23 receptor (IL23R) polymorphisms and haplotypes with rheumatoid arthritis (RA). The study was conducted on 1,204 RA patients and 979 healthy controls. Seven polymorphisms were selected from previous IBD reports. The seven SNPs (rs1004819, rs7517847, rs10489629, rs2201841, rs1343151, rs11209032 and rs1495965) were genotyped using the TaqMan assay. Comparison of RA and control subjects revealed no statistically significant differences in the distribution of the IL23R genotypes and haplotypes. Our results clearly indicate that IL23R gene polymorphisms do not play a significant role in susceptibility to RA in the Korean population. Accordingly, we conclude that IL23R gene polymorphisms cannot be applied as an effective genetic marker for RA susceptibility.

    PMID:
    19034457
    [PubMed - indexed for MEDLINE]

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