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• TLRs may play a role in the pathogenesis of psoriasis. • In our study, we have demostrated a new SNP which might associate with susceptibility to psoriasis in the Turkish population. • rs4696480 SNP with psoriasis was examined. Toll-like receptors (TLRs) have an important role in the host defense. Recent studies demonstrated that TLR polymorphisms might have a role in the pathogenesis of psoriasis vulgaris. The aim of this study was to indicate whether TLR2 rs11938228 and rs4696480 were associated with susceptibility to psoriasis in the Turkish population. This case-control study included 140 psoriasis patients and 250 controls. Genotyping of 2 rs11938228 and rs4696480 SNPs of TLR2 were determined using LightSNiP Kit (Roche Diagnostic, GmBH, Mannheim, Germany). Our results demonstrated that the TLR2 -rs4696480 AA genotype seemed to have a higher risk for psoriasis [crude 95% CI: 1.495–4.514, and p < 0.001, adjusted 95% CI: 1.349–4.292, and p = 0.003] while as TLR2 -rs11938228 polymorphism has not shown any significant association with the risk of psoriasis [p > 0.005]. There was no statistically significant difference between the mean age, gender, onset age, and PASI level and genotypes for rs11938228 and rs4696480 polymorphisms (p > 0.05). The SNP rs4696480 of TLR2 may have significant effects on the heritability of psoriasis in the Turkish population. [ABSTRACT FROM AUTHOR]

Toll-like receptors (TLRs) play an important role in the induction and regulation of the innate immune system or adaptive immune responses. Genetic variations within human TLRs have been reported to be associated with a range of immune-related diseases. This study was conducted to investigate the frequencies of TLR3 rs3775290, TLR9 rs187084, and TLR10 rs4129009 polymorphisms and to detect between polymorphisms and autoantibody positive as RF, collagen type II, anti-RNP, and anti-CCP in patient group. We performed a case-control study of 100 rheumatoid arthritis (RA) cases and 100 healthy controls matched on age, sex, and residence. All polymorphisms in TLRs were determined by polymerase chain reaction-based restriction fragment length polymorphism. Serum autoantibody level was measured using quantitative ELISA. SNPs were genotyped in all samples. Our results showed that TT genotype for SNP 1237 T/C increased the RA risk significantly ( p < 0.05). No statistically significant differences were found in the TLR3 and TLR10 genotypes or allele distribution between RA patients and control individuals. No associations were noted with autoantibody production and TLR3, TLR9, and TLR10 polymorphisms genotypes ( p > 0.05). Our study suggests that a single nucleotide polymorphism (rs187084) in TLR9 gene may be a susceptibility factor for RA in Turkish population. Further studies are required to explore the role of TLRs gene polymorphisms in the risk of RA, especially in ethnically different populations to confirm our results. [ABSTRACT FROM AUTHOR]