The ST2 rs3821204 CC genotype was associated with a significantly increased risk of HCC (CC vs. GG: adjusted OR = 2.29, 95% CI, 1.39-3.78; dominant model: adjusted OR = 1.58, 95% CI, 1.12-2.23; recessive model: adjusted OR = 1.88, 95% CI, 1.21-2.93; C vs. G: adjusted OR = 1.53, 95% CI, 1.20-1.95).
These findings suggest that the rs7025417 and rs3821204 may have a combined effect to protect against the development of OS by decreasing the expression levels of IL-33 or ST2.
Taken together, our findings provide the first evidence that genetic variants in ST2 gene are associated with EH risk and variant rs3821204 may influence the development of EH by controlling sST2 expression.
Statistically significant allelic associations with CRS were noted for 5 SNPs (rs10204137, p = 0.04; rs10208293, p = 0.03; rs13431828, p = 0.008; rs2160203, p = 0.03, and rs4988957, p = 0.03).
Our data indicate that IL1RL1 SNPs rs6543115(C) confer susceptibility to UC an</span>d is contained in the GRE, which may modulate glucocorticoid-induced sST2 expression.
Sequencing of a distal IL1RL1 promoter region demonstrated that SNPs rs6543115(C) and rs6543116(A) are associated with increased sST2 in UC patients on corticosteroids.
The frequencies of allele A and AA+AG genotype of rs6543116 (ST2) in HT patients were significantly increased compared with those of the controls (P = 0.029/0.021, OR = 1.31/1.62).
Our study showed that variants rs11685424, rs12999364 and rs3821204 are highly associated with an increase in risk of EH, while rs6543116 is associated with a decrease risk of EH.
We also identified two genome-wide significant associations: rs13408661 near IL1RL1/IL18R1 (P(Stage1+Stage2) = 1.1x10(-9)), which is correlated with a variant recently shown to be associated with asthma (rs3771180), and rs9268516 in the HLA region (P(Stage1+Stage2) = 1.1x10(-8)), which appears to be independent of previously reported associations in this locus.