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DOI 10.1111/eci.13199

Медицинская библиотека · European journal of clinical investigation · 2020

DNA methylation analysis within the IL2RA gene promoter in youth with autoimmune thyroid disease.

Kyrgios Ioannis, Fragou Aikaterini, Kotanidou Eleni P, Mouzaki Konstantina, Efraimidou Smaragda, Tzimagiorgis Georgios, Galli-Tsinopoulou Assimina

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Аннотация

BACKGROUND

Alpha-subunit of the interleukin-2 receptor (IL2RA) is involved in the regulation of T-cell function and has been related to autoimmune thyroid disease (AITD). Although the exact mechanisms are not fully understood, promoter methylation might account for differences in gene expression. The aim of this study was to investigate whether there are differences in the percentage of DNA methylation within the IL2RA gene promoter in young patients with AITD.

MATERIALS AND

METHODS

In a cross-sectional design, the presence of DNA methylation in the IL2RA gene promoter was quantified, by real-time PCR and melting curve analysis, in modified genomic DNA isolated from blood samples of a total of 149 children and adolescents with AITD, including patients with Hashimoto thyroiditis (ΗΤ) (n = 60), Graves' disease (GD) (n = 9), concurrent diagnosis of HT and type 1 diabetes (T1DM + HT) (n = 25), and healthy controls (n = 55).

RESULTS

The percentage of DNA methylation in the IL2RA gene promoter was significantly decreased in patients with GD (26.0 ± 4.2%) but not in those with HT (36.3 ± 1.4%) in comparison with controls (41.3 ± 1.5%).

CONCLUSIONS

The observed DNA hypomethylation in the IL2RA gene promoter in patients with GD might be related to its increased expression, thus contributing to the etiopathogenesis of GD in childhood and adolescence.

Для цитирования: Kyrgios Ioannis, Fragou Aikaterini, Kotanidou Eleni P, Mouzaki Konstantina, Efraimidou Smaragda, Tzimagiorgis Georgios, Galli-Tsinopoulou Assimina. DNA methylation analysis within the IL2RA gene promoter in youth with autoimmune thyroid disease.. European journal of clinical investigation. 2020. DOI: 10.1111/eci.13199.

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