Abstract
The association between the IL-23R and IL-17A polymorphisms and ankylosing spondylitis (AS) in the Southwest Chinese Population is still unclear. The purpose of this study is to detect the association between IL-23R and IL-17A polymorphisms and AS. A case–control study consisting of 486 AS patients and 480 healthy controls was performed. We used the high-resolution melting methods (HRM) to genotype five selected single nucleotide polymorphisms (SNPs), rs6693831, rs7517847, rs1884444, rs10889677 in the IL-23R gene and rs2275913 in the IL-17A gene. Meanwhile, the laboratory indexes were recorded. In this study, patients with genotype CC (p = 8.574E-8) and allele C (p = 3.206E-31) on SNP rs6693831 (IL-23R) showed decreased risk of AS. The genotype TT (p = 4.551E-6) and allele T (p = 0.02) on SNP rs1884444 (IL-23R) showed significant lower risk of AS. Individuals carrying the allele A of rs2275913 showed higher morbidity of AS (p = 0.04). We first detected that rs6693831 and rs1884444 in IL-23R gene and rs2275913 in IL-17A gene have genetic association with AS.
Highlights
Ankylosing spondylitis (AS), the most common form of spondyloarthropathy, is an insidiously progressive multi-system inflammatory disorder
For the other two single nucleotide polymorphisms (SNPs) in Interleukin 23 receptor (IL-23R), no significant difference was observed between AS patients and healthy controls. (Table 1)
The results above indicate that IL-23R and IL-17A correlate with AS susceptibility in a Chinese Han population
Summary
Ankylosing spondylitis (AS), the most common form of spondyloarthropathy, is an insidiously progressive multi-system inflammatory disorder. AS typically causes back pain, lesion of the sacroiliac joints and axial skeleton, the most common lesion is inflammation on fibrous or fibro-cartilaginous structures [1]. Osteoproliferation leads to the ossification of ligaments, tendons and joint capsules, and eventually to ankyloses [2, 3]. Besides the best known risk factor HLA-B27 (Human Leukocyte Antigen B27), the non-major histocompatibilitycomplex susceptibility loci such as endoplasmic reticulum aminopeptidase 1 (ERAP1) and IL-23R (interleukin 23 receptor) have been confirmed to contribute to the total genetic risk [5,6,7]. With the success of genome-wide association studies (GWAS) in recent years, many single nucleotide polymorphisms (SNPs) are identified with genetic contributions to the disease [8]
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