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Abstract
Classical genetic studies established a link between Type 1 diabetes, a common childhood autoimmune disease and genes that encode MHC antigens and several immune-related determinants. The mechanisms by which these genes contribute to the initiation and perpetuation of Type 1 diabetes remain enigmatic. Emerging data indicate a role for epigenetic mechanisms involving hyperacetylation of histones in the differential gene expression and amelioration of autoimmune diabetes in a mouse model. In this article the implications of these and other epigenetic mechanisms including ncRNA-mediated gene regulation in the abrogation of autoimmune diabetes are discussed. Concerted efforts to decipher the epigenetics of Type 1 diabetes may provide novel perspectives on autoimmune diabetogenesis.
Acknowledgements
The author acknowledges the contribution of many members of his laboratory to the work cited in this article.
Financial & competing interests disclosure
The author has no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.
No writing assistance was utilized in the production of this manuscript.