RESUMEN

Interleukin-23 receptor (IL-23R) and signal transducer and activator of transcription 3 (STAT3) polymorphisms are common risk factors for a number of T helper (Th) 17-mediated autoimmune diseases. However, the importance of genetic variations in Th17 pathways to thyroid autoimmunity, and particularly Hashimoto's thyroiditis (HT), is not fully understood. In this study, we genotyped three single nucleotide polymorphisms (SNPs) within the IL-23R (rs11209026/p.Arg381Gln, rs7530511) and STAT3 (rs744166) genes in 217 Croatian patients with HT and 161 healthy controls using fluorescence resonance energy transfer technology and melting curve analysis of polymerase chain reaction products. None of the tested SNPs or IL-23R haplotypes was associated with HT susceptibility or disease severity. These results suggest that the studied IL-23R/STAT3 polymorphisms affecting Th17 signaling efficiency are not major determinants of HT risk in the Croatian population. Further work is necessary to determine if these loci contribute modestly or conditionally to the risk of HT.

Asunto(s)

Enfermedad de Hashimoto/genética , Polimorfismo de Nucleótido Simple , Receptores de Interleucina/genética , Factor de Transcripción STAT3/genética , Adulto , Sustitución de Aminoácidos , Estudios de Casos y Controles , Estudios de Cohortes , Croacia , Femenino , Estudios de Seguimiento , Estudios de Asociación Genética , Predisposición Genética a la Enfermedad , Enfermedad de Hashimoto/tratamiento farmacológico , Enfermedad de Hashimoto/metabolismo , Enfermedad de Hashimoto/fisiopatología , Terapia de Reemplazo de Hormonas , Humanos , Masculino , Persona de Mediana Edad , Proyectos Piloto , Receptores de Interleucina/metabolismo , Factor de Transcripción STAT3/metabolismo , Índice de Severidad de la Enfermedad , Tiroxina/uso terapéutico