The combination of ınterleukin-10 − 1082 and tumor necrosis factor α − 308 or ınterleukin-6 − 174 genes polymorphisms suggests an association with susceptibility to Hashimoto's thyroiditis

BackgroundThe etiopathogenesis of Hashimoto's thyroiditis (HT) has not been clearly elucidated although the role of chronical inflammation and endothelial dysfunction has been established. The imbalance between pro- and anti-inflammatory cytokines may play a role in the etiology. The aim of the present study was to investigate whether cytokine gene polymorphisms are associated with HT, and to evaluate the relationship between genotypes and clinical/laboratory manifestation of HT.MethodsTumor necrosis factor α (TNFα) G-308A (rs 1800629), interleukin-6 (IL-6) G-174C (rs 1800795) and IL-10 G-1082A (rs 1800896) single nucleotide polymorphisms (SNPs) in DNA from peripheral blood leukocytes of 190 patients with HT and 231 healthy controls were investigated by real-time PCR combined with melting curve analysis using fluorescence-labeled hybridization probes.ResultsThere was no notable risk for HT afflicted by TNFα − 308, IL-6 − 174 and IL-10 − 1082 polymorphisms alone. However, carriers of variant alleles of both IL-10 − 1082 and TNFα − 308 polymorphisms had four-fold times higher risk for HT in comparison with non-carriers. Additionally, concomitant presence of both mutant IL-10 − 1082 A and IL-6 − 174 C alleles raised three-fold the HT risk.ConclusionOur results suggest that the combined effects of TNFα − 308, IL-6 − 174 and IL-10 − 1082 variant alleles may be more decisive to induce functional differences and modify the risk for HT.

► We investigated the possible relationship between cytokine polymorphisms and HT ► TNFα G-308A, IL-6 G-174C, IL-10 G-1082A polymorphisms were assayed by real-time PCR ► The TNFα − 308, IL-6 − 174, IL-10 − 1082 polymorphisms are not risk factors for HT alone ► The concomitant presence of mutant IL-10/TNFα, IL-10/IL-6 alleles rised risk for HT