Article ID Journal Published Year Pages File Type
5834150 International Immunopharmacology 2012 4 Pages PDF
Abstract

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

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