Lack of association between interleukin 23 receptor gene polymorphisms and rheumatoid arthritis susceptibility
- Authors
- Park, Jeong Ha; Kim, Yun Jung; Park, Byung Lae; Bae, Joon Seol; Shin, Hyoung Doo; Bae, Sang-Cheol
- Issue Date
- May-2009
- Publisher
- SPRINGER HEIDELBERG
- Keywords
- Rheumatoid arthritis (RA); Interleukin 23 (IL-23); Interleukin 23 receptor (IL23R); Polymorphism; Susceptibility
- Citation
- RHEUMATOLOGY INTERNATIONAL, v.29, no.7, pp.781 - 786
- Indexed
- SCIE
SCOPUS
- Journal Title
- RHEUMATOLOGY INTERNATIONAL
- Volume
- 29
- Number
- 7
- Start Page
- 781
- End Page
- 786
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/176818
- DOI
- 10.1007/s00296-008-0770-x
- ISSN
- 0172-8172
- 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.
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