Abstract
Epigenetics of asthma and allergic disease is a field that has expanded greatly in the last decade. Previously thought only in terms of cell differentiation, it is now evident the epigenetics regulate many processes. With T cell activation, commitment toward an allergic phenotype is tightly regulated by DNA methylation and histone modifications at the Th2 locus control region. When normal epigenetic control is disturbed, either experimentally or by environmental exposures, Th1/Th2 balance can be affected. Epigenetic marks are not only transferred to daughter cells with cell replication but they can also be inherited through generations. In animal models, with constant environmental pressure, epigenetically determined phenotypes are amplified through generations and can last up to 2 generations after the environment is back to normal. In this review on the epigenetic regulation of asthma and allergic diseases we review basic epigenetic mechanisms and discuss the epigenetic control of Th2 cells. We then cover the transgenerational inheritance model of epigenetic traits and discuss how this could relate the amplification of asthma and allergic disease prevalence and severity through the last decades. Finally, we discuss recent epigenetic association studies for allergic phenotypes and related environmental risk factors as well as potential underlying mechanisms for these associations.
Highlights
The term epigenetics was coined by C.H
The concept of epigenetics was initially limited to cell differentiation from pluripotent stem cells to unipotent well differentiated cells, but the modern definition of epigenetics has been broaden beyond differentiation to include non-sequence inheritance
The purpose of this review is to provide allergy/immunology professionals and researchers with a broad, yet easyto-follow, review of the epigenetic regulation of asthma and allergic disease
Summary
The term epigenetics was coined by C.H. Waddington in the 1950’s to describe means in addition to genetics to explain cell differentiation [1]. Since epigenetic marks have the potential to silence a gene, it is to be expected that it can modulate the effect of an Figure 6 Loci identified from previous DNA methylation association studies for asthma, atopy and related exposures. Exposure to tobacco smoke has been shown to alter the expression of dnmt and dnmt3b [106] Both tobacco smoke and pollution induce oxidative stress which are thought to favour the demethylation process, as well as to cause lesions to DNA which prevent binding of Dnmt, resulting in a non-specific decrease in methylation across the genome [107,108,109]. Whether the previously reported protective effect of antioxidant supplement can be related to an effect on DNA demethylation is still undetermined [113,114,115,116]
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