Are single nucleotide polymorphisms in the IL-2 gene biomarkers for Hashimoto's thyroiditis?

(HT) is an autoimmune disorder that can lead to hypothyroidism. The pathophysiology of HT involves the production of antithyroid antibodies that attack the thyroid tissue, causing inflammation and progressive fibrosis. Recent studies demonstrated a strong correlation between Interleukin-2 (IL-2) levels and the development of autoimmune diseases, suggesting that this cytokine may play a crucial role in the pathogenesis of HT. In this study, we determined the presence of the point mutation +114T/G in the gene in patients with HT compared with a control group, and also the serum level of anti-thyroid peroxidase (TPOAbs) and anti-thyroglobulin (TgAbs) antibodies in HT patients with vs. without the mutation. The sequences of the gene obtained from subjects were determined by the Sanger sequencing method. Our study did not reveal that the +114T/G polymorphism of the gene is a susceptibility or protective factor for HT. No significant correlations were observed between the reference genotype, hetero- and homozygous +114T/G polymorphism and TPOAbs, respectively TgAbs serum levels in HT patients. Further studies of more cases are needed to identify more polymorphisms in the gene and study their correlations with HT.