Journal of Thyroid Disorders & Therapy
Open Access

Exploring Epigenetic Modifications in Autoimmune Thyroid Disorders

Patricia Elizabeth^{* *}Correspondence: Patricia Elizabeth, Department of Medicine, University of Minnesota, Minneapolis, USA, Email:

Author info »

Description

Thyroid dysfunction is frequently caused by Autoimmune Thyroid Diseases (AITDs), such as Graves' disease and Hashimoto's thyroiditis. These conditions result from the immune system wrongly attacking the thyroid gland, which damages tissue, causes inflammation and impairs thyroid function. Although the exact origins of AITDs remain unclear, an increasing amount of data points to the critical role that epigenetic changes play in the onset and progression of these disorders. The term "epigenetics" describes modifications to gene expression that do not include changes to the underlying DNA sequence. Rather, the pathophysiology of autoimmune diseases is influenced by these alterations, which are caused by DNA methylation, histone modifications and non-coding RNAs.

In autoimmune thyroid diseases, both genetic predisposition and environmental factors are thought to contribute to disease onset and epigenetic modifications offer a mechanism by which these factors may interact. These modifications can influence the immune response, potentially tipping the balance toward autoimmunity. In AITDs, altered DNA methylation patterns have been observed in immune-related genes, including those involved in thyroid function and immune regulation. These changes may affect the expression of key genes that regulate immune tolerance, thereby promoting an autoimmune response against thyroid antigens. Another essential epigenetic process is histone modification, which involves the addition or deletion of chemical groups (like acetyl or methyl groups) to the histone proteins that encircle DNA. Gene expression may be impacted by these changes in chromatin structure. A number of disorders, including Graves' disease and Hashimoto's thyroiditis, may be attributed to specific alterations that increase the production of autoantibodies or pro-inflammatory cytokines. Genetically predisposed people's immune responses can also be impacted by environmental variables including infections, stress and food, which can alter histone alterations.

In autoimmune disorders, non-coding RNAs in particular, microRNAs have also been shown to be significant modulators of gene expression. By attaching to messenger RNAs (mRNAs) and blocking their translation, these tiny RNA molecules alter the expression of target genes rather than coding for proteins. Changes in microRNA expression have been connected to the emergence of autoimmune reactions in AITDs. For example, T helper cells, which are essential for the development of autoimmunity, are immune cells whose activity may be controlled by certain microRNAs. These microRNAs may have a role in the dysregulated immune responses observed in autoimmune thyroid disorders by affecting immune cell activity and pro-inflammatory cytokine production. The possible reversibility of epigenetic changes in AITDs is among its most alluring features. Epigenetic modifications can be dynamic and sensitive to environmental cues, in contrast to genetic mutations, which are irreversible. This suggests that treatment strategies may target epigenetic changes. For instance, medications that alter histones or DNA methylation are being researched for their potential to treat autoimmune disorders. Epigenetic medications have demonstrated promise in reestablishing healthy immune function and slowing the course of AITDs in animal studies. Furthermore, lifestyle modifications like stress reduction or dietary adjustments may have an impact on epigenetic regulation and provide a means of lowering the incidence or severity of autoimmune thyroid diseases. Even though the connection between epigenetics and autoimmune thyroid disorders is becoming more well acknowledged, many concerns still need to be addressed. Determining the precise processes behind AITDs is difficult because to the complex interaction between genetic predisposition, environmental variables and epigenetic alterations.

Conclusion

An essential component in comprehending the pathophysiology of autoimmune thyroid diseases is epigenetic changes. These changes can affect thyroid-specific gene expression, immune cell function, and the immune response as a whole, which can lead to the onset of conditions including Graves' disease and Hashimoto's thyroiditis. There is still much to learn about the exact processes behind these disorders, despite the fact that great strides have been made in determining the roles of DNA methylation, histone modifications and non-coding RNAs.