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

• DOI: 10.1007/s00005-017-0473-7
• Publication Date: 2017-05-25T15:52:03Z
• Authors: Isaura Isabelle F...; Hildson Dornelas ...; Eliezer Rushansky; Maria Helena Mariano; Maria de Mascena ...; Paulo Roberto Ele...
• Keywords: Adult; Aged, 80 and over; Male; 0301 basic medicine; Genotype; Interleukin-17; Receptors, Interleukin; Middle Aged; Polymorphism, Single Nucleotide; 3. Good health; Arthritis, Rheumatoid; Young Adult; 03 medical and health sciences; Gene Frequency; Case-Control Studies; Humans; Th17 Cells; Female; Genetic Predisposition to Disease; Brazil; Genetic Association Studies

Rheumatoid 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/C IL-23R (rs10889677), -197 G/A IL-17A (rs2275913), and +7488 A/G IL-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 the IL-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/A IL-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/G IL-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/C IL-23R and -197 G/A IL-17A could contribute to RA development in the studied population. However, larger studies are needed to fully understand this genetic predisposition.