Abstract
Autoimmune thyroid diseases (AITD) are a group of both B cell- and T cell-mediated organ-specific autoimmune diseases. Graves’ disease and Hashimoto thyroiditis are the two main clinical presentations of AITD. Both genetic and environmental factors have important roles in the development of AITD. Epigenetics have been considered to exert key roles in integrating those genetic and environmental factors, and epigenetic modifications caused by environmental factors may drive genetically susceptibility individuals to develop AITD. Recent studies on the epigenetics of AITD have provided some novel insights into the pathogenesis of AITD. The aim of this review is to provide an overview of recent advances in the epigenetic mechanisms of AITD, such as DNA methylation, histone modifications, and non-coding RNAs. This review highlights the key roles of epigenetics in the pathogenesis of AITD and potential clinical utility. However, the epigenetic roles in AITD are still not fully elucidated, and more researches are needed to provide further deeper insights into the roles of epigenetics in AITD and to uncover new therapeutic targets. Although there are many studies assessing the epigenetic modifications in AITD patients, the clinical utility of epigenetics in AITD remains poorly defined. More studies are needed to identify the underlying epigenetic modifications that can contribute to accurate diagnosis of AITD, adequate choice of treatment approach, and precise prediction of treatment outcomes.
Highlights
Autoimmune thyroid diseases (AITD) are a group of both B cell- and T cell-mediated autoimmune diseases, which are caused by loss of immune tolerance and autoimmune attack to thyroid tissues [1, 2]
The aim of this review is to provide an overview of recent advances in the epigenetic mechanisms of AITD, to highlight the epigenetic roles in the pathogenesis of AITD, and to discuss the potential clinical utility of epigenetic modifications in AITD
A recent study by Ishido at al. reported that there was no obvious difference of skewed X Chromosome Inactivation (XCI) between AITD cases and controls, but it was significantly higher in intractable Graves’ disease (GD) patients (66.7%) than those with GD remission (25.0%), which suggested that skewed XCI was related to the GD progression [188]
Summary
Bin Wang1,2†, Xiaoqing Shao1,2†, Ronghua Song, Donghua Xu3 and Jin-an Zhang1,2*. Specialty section: This article was submitted to Immunological Tolerance and Regulation, a section of the journal Frontiers in Immunology. Graves’ disease and Hashimoto thyroiditis are the two main clinical presentations of AITD. Both genetic and environmental factors have important roles in the development of AITD. Epigenetics have been considered to exert key roles in integrating those genetic and environmental factors, and epigenetic modifications caused by environmental factors may drive genetically susceptibility individuals to develop AITD. Recent studies on the epigenetics of AITD have provided some novel insights into the pathogenesis of AITD. The aim of this review is to provide an overview of recent advances in the epigenetic mechanisms of AITD, such as DNA methylation, histone modifications, and non-coding RNAs. This review highlights the key roles of epigenetics in the pathogenesis of AITD and potential clinical utility.
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