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

Eur J Clin Invest

4th Department of Pediatrics, Medical School, Faculty of Health Sciences, Aristotle University of Thessaloniki, Papageorgiou General Hospital, Thessaloniki, Greece.

Published: March 2020

AI Article Synopsis

  • The IL2RA gene plays a role in regulating T-cell function and may be linked to autoimmune thyroid disease (AITD) through promoter methylation differences.
  • A study measured DNA methylation in the IL2RA promoter using blood samples from 149 young patients with AITD and healthy controls.
  • Results indicated significantly lower DNA methylation in patients with Graves' disease, which may enhance gene expression and affect the development of the disease in children and adolescents.

Article Abstract

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.

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http://dx.doi.org/10.1111/eci.13199DOI Listing

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