Interleukin (IL)-23 Receptor, IL-17A and IL-17F Gene Polymorphisms in Brazilian Patients with Rheumatoid Arthritis

AbstractRheumatoid arthritis (RA) is a progressive, autoimmune disease for which the previous studies have shown that some functional polymorphisms can influence its etiology. Knowing this, the aim of this study was to investigate the association of +2199 A/CIL-23R (rs10889677), −197 G/AIL-17A (rs2275913), and +7488 A/GIL-17F (rs763780) gene polymorphisms with RA susceptibility and clinical features in a Brazilian population. A total of 127 RA patients and 134 healthy controls were recruited for the analyses of polymorphic variants. Genotyping was performed using RFLP-PCR. Logistic regression was used to analyze the genotype distribution of the polymorphisms. Individuals carrying the homozygous CC genotype for theIL-23R polymorphism seem to be at lower risk for RA development (OR 0.22;p = 0.004), as well as those carrying the variant C allele (OR 0.56;p = 0.002). For the −197 G/AIL-17A polymorphism, the wild-type genotype (GG) was significantly associated with a 3.18-fold (OR 3.18;p = 0.033) increased risk for RA. In relation to the +7488 A/GIL-17F polymorphism, no significant difference was found between RA cases and control subjects (p >  0.05). Moreover, when investigating the relationship between polymorphisms and clinical features, no evidence of an association was found. Our findings suggest that the variants +2199 A/CIL-23R and −197 G/AIL-17A could contribute to RA development in the studied population. However, larger studies are needed to fully under...
Source: Archivum Immunologiae et Therapiae Experimentalis - Category: Allergy & Immunology Source Type: research