title: 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.
abstract: BACKGROUND
  The 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.
  
  
  METHODS
  Tumor 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.
  
  
  RESULTS
  There 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.
  
  
  CONCLUSIONS
  Our 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.
authors.affiliation: Department of Biochemistry, Istanbul Faculty of Medicine, Istanbul University, Çapa, Istanbul, Turkey.
authors.forename: Merve
authors.initials: M
authors.lastname: Baki
authors.forename: Fevziye E
authors.initials: FE
authors.lastname: Akman
authors.forename: Pervin
authors.initials: P
authors.lastname: Vural
authors.forename: Semra
authors.initials: S
authors.lastname: Doğru-Abbasoğlu
authors.forename: Ayşenur
authors.initials: A
authors.lastname: Özderya
authors.forename: Berrin
authors.initials: B
authors.lastname: Karadağ
authors.forename: Müjdat
authors.initials: M
authors.lastname: Uysal
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D005260:Female; D020022:Genetic Predisposition to Disease; D050031:Hashimoto Disease / Q000235:genetics*; D006801:Humans; D016753:Interleukin-10 / Q000235:genetics*; D015850:Interleukin-6 / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D011110:Polymorphism, Genetic; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics*; D055815:Young Adult
chemical_list: D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10