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Review
. 2021 Jun 8;12(6):887.
doi: 10.3390/genes12060887.

Epigenetic Changes Induced by Maternal Factors during Fetal Life: Implication for Type 1 Diabetes

Affiliations
Review

Epigenetic Changes Induced by Maternal Factors during Fetal Life: Implication for Type 1 Diabetes

Ilaria Barchetta et al. Genes (Basel). .

Abstract

Organ-specific autoimmune diseases, such as type 1 diabetes, are believed to result from T-cell-mediated damage of the target tissue. The immune-mediated tissue injury, in turn, is known to depend on complex interactions between genetic and environmental factors. Nevertheless, the mechanisms whereby environmental factors contribute to the pathogenesis of autoimmune diseases remain elusive and represent a major untapped target to develop novel strategies for disease prevention. Given the impact of the early environment on the developing immune system, epigenetic changes induced by maternal factors during fetal life have been linked to a likelihood of developing an autoimmune disease later in life. In humans, DNA methylation is the epigenetic mechanism most extensively investigated. This review provides an overview of the critical role of DNA methylation changes induced by prenatal maternal conditions contributing to the increased risk of immune-mediated diseases on the offspring, with a particular focus on T1D. A deeper understanding of epigenetic alterations induced by environmental stressors during fetal life may be pivotal for developing targeted prevention strategies of type 1 diabetes by modifying the maternal environment.

Keywords: DNA methylation; autoimmune diseases; epigenetics; genomic imprinting; maternal factors; type 1 diabetes.

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Conflict of interest statement

The authors declare no competing financial interest. The funders had no role in the study design, data collection and analysis, decision to publish, or manuscript preparation.

Figures

Figure 1
Figure 1
Schematic illustrating the proposed role of epigenetics as a link between genetic and environmental factors in the autoimmune destruction of the pancreatic beta cells.

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