IL23R Gene Polymorphisms in the Chinese Han Patients with Behcet’s Disease, Vogt-Koyanagi-Harada Syndrome and Fuchs’ Syndrome
|School||Chongqing Medical University|
|Keywords||Behcet's disease Vogt- Koyanagi -Harada syndrome IL23R Polymorphic Correlation Fuchs syndrome|
Objective: interleukin 23 receptor (IL23R) in a recent study popular IL23/IL17 this pathway plays an important role. IL23 and IL23R combined activation TH17 cells secrete inflammatory cytokines IL17 this important. Our group studies show: IL23/IL17 pathway in Behcet's disease and Vogt-Koyanagi-Harada syndrome occurrence and development plays an important role. Recent studies have found IL23R polymorphism with Crohn's disease, vitiligo and other autoimmune diseases related. Therefore, the present study was to investigate whether the IL23R gene polymorphism in Han Chinese Behcet's disease, Vogt-Koyanagi-Harada syndrome and Fuchs' syndrome. Methods: PCR-RFLP and sequencing analysis of 338 cases of Behcet patients, 382 cases of Vogt-Koyanagi-Harada syndrome, 138 cases of Fuchs syndrome and 407 normal controls IL23R gene over four polymorphic loci (rs17375018, rs7517847, rs11209032, rs1343151 ) for genotyping. Results: The normal IL23R gene 4 SNP genotyping results in Hardy Weinberg equilibrium, p greater than 0.05. Behcet disease patients IL23R gene rs11209032 AA genotype and rs17375018 GG genotype frequencies were significantly higher (p = 0.024, OR 1.69,95% CI 1.21 ~ 2.35; p lt; 0.001, OR 1.86,95% CI 1.39 ~ 2.49); rs11209032 A allele of rs17375018 G allele frequency was higher (p lt; 0.001, OR 1.48,95% CI 1.21 ~ 1.82; p lt; 0.001, OR 1.57,95% CI 1.25 ~ 1.98). In IL23R gene rs1343151 and rs7517847 allele and genotype frequencies, Behcet patients and normal control group were not significantly different. Haplotype analysis showed that: in Behcet patients who, rs17375018 A, rs7517847G, rs1343151C and rs11209032G haplotype frequencies were significantly lower than the control group (p lt; 0.001, OR 0.59,95% CI 0.45 ~ 0.77). While the other haplotype frequencies in patients and normal controls were not statistically different between groups. Normal IL23R gene 4 SNP genotyping results in Hardy Weinberg equilibrium, p greater than 0.05. Vogt-Koyanagi-Harada syndrome IL23R gene 4 SNP allele, genotype and haplotype frequencies and normal control group were not statistically different between. Normal control group IL23R gene 3 SNP (rs11209032, rs17375018 and rs7517847) genotyping results meet the Hardy Weinberg equilibrium, p values ??were greater than 0.05. rs11209032 genotype frequencies of AA in Fuchs' syndrome patients was significantly higher than normal controls (pc = 0.036, OR 1.86, 95% CI 1.21-2.86). Studied IL23R gene loci other genotype and allele frequencies in patients and normal controls were not statistically different between groups. Conclusion: IL23R gene polymorphism with Behcet's disease pathogenesis. rs11209032 and rs17375018 AA genotype GG loci may be Behcet's disease susceptibility genes, while rs17375018 A, rs7517847G, rs1343151C and rs11209032G Behcet disease haplotype is prompted protective factors. IL23R gene polymorphisms and Vogt-Koyanagi-Harada syndrome no correlation. IL23R gene polymorphisms and Fuchs syndrome.