4.5 Article

Association between IL-18 gene polymorphisms and Hashimoto thyroiditis

Journal

MOLECULAR BIOLOGY REPORTS
Volume 48, Issue 10, Pages 6703-6708

Publisher

SPRINGER
DOI: 10.1007/s11033-021-06659-5

Keywords

Hashimoto's thyroiditis; Interleukin 18 gene polymorphism; -137 IL18 CG genotype; -607 AC genotype

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The study found an association between IL-18 gene polymorphisms and Hashimoto's thyroiditis, with the CG genotype being a potential risk factor for HT and the AC genotype possibly playing a protective role. Further research will contribute to understanding the molecular and cellular mechanisms of HT.
Background Hashimoto's thyroiditis (HT), which is also called lymphocytic thyroiditis, is the most frequent autoimmune thyroid disease (AITD), in which T helper-1 lymphocytes mediate the disease. IL-18 is expressed in thyroid follicular cells (TFCs) during HT. The findings of studies aimed at investigating the relationship between IL-18 and HT are highly contradictory. In this study, we aimed to investigate the association between IL-18 gene polymorphisms and HT. Methods and results The study included 97 patients diagnosed with HT and 86 volunteers in the healthy control group. The IL18-607C/A (rs1946518) and -137G/C (rs187238) genotypes were determined using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. No significant difference in the mean age or sex was observed between the groups (p = 0.763 and p = 0.658, respectively). The -137 IL18 CG genotype was more frequent in HT patients than in controls. In HT patients, the risk of the IL-18 CG genotype was more than 2.237 times higher (OR 2.237%95 Cl 1.195-4.187, p = 0.039) than that of the G/G genotype. Additionally, the -607 AC genotype was more frequent in the control group than in the HT group (in individuals with the IL18 CG genotype). Conclusions According to our results, the CG genotype might be a risk factor for HT. Conversely, there is a possibility that the AC genotype plays a protective role against the condition. However, further studies will contribute to new solutions by revealing the molecular and cellular mechanisms of HT.

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