Background The association between the IL-23R and IL-17A polymorphisms and ankylosing spondylitis (AS) in a Chinese Han population is still unclear.
Objectives The purpose of this study is to detect the association between IL-23R and IL-17A polymorphisms and AS.
Methods 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 the selected five single nucleotide polymorphisms (SNPs), four of them (rs6693831, rs7517847, rs1884444, rs10889677) on the IL-23R gene and one (rs2275913) on the IL-17A gene. Meanwhile the laboratory indexes (RBC, WBC, PLT, MONO%, LYMPH%, NEUT%, ALB, ALP, ALT, AST, BUN, CHOL, CK, CREA, Cys-C, DBIL, GGT, GLB, GLU, HBDH, HDL-C, IBIL, LDH, LDL-C, TBIL, CRP, C3 and C4) were recorded.
Results 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 on SNP rs2275913 (IL-17A) showed higher risk of AS [p=0.04, OR (95%CI) = 0.825 (0.690–0.987)]. Significant higher level of CRP was found among AS patients with genotype CT on rs6693831 (χ2=7.633, P=0.030).
Conclusions We first demonstrated that rs6693831 and rs1884444 on IL-23R gene and rs2275913 on IL-17A gene are genetic susceptibility factor for AS. We also noticed that patients with CT genotype on rs6693831 have higher CRP level.
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Acknowledgement We are grateful to the participating AS patients and their families. This research was sponsored by the National Natural Science Foundation of China (Nos. 81301496, and 81202354). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Disclosure of Interest B. Yang Shareholder of: No, Grant/research support from: No, Consultant for: No, Employee of: No, Paid instructor for: No, Speakers bureau: No, J. Chen: None declared, L. Wang: None declared