Abstract

For several decades the incidence and prevalence of chronic inflammatory diseases have been increasing, particularly in westernized countries. These diseases include allergic conditions (asthma, eczema) as well as autoimmune diseases. It is now well established that the development of clinical phenotypes is the result of an intimate interaction between genetic predisposition and environmental exposures. The adaptive immune system plays an important role in orchestrating the inflammatory response. In this regard, T-helper cell differentiation into Th1, Th2, Th17, Treg and other T-cell subsets plays an important role. Recent data further indicate that there is a high degree of flexibility and plasticity among these effector cells. T-helper cell differentiation is tightly controlled by epigenetic mechanisms. These include DNA methylation, histone acetylation and the role of microRNA. Epigenetic regulation represents an important mode of action for environmental factors – including nutritional agents, stress and microbial compounds – to regulate gene expression resulting in disease development.

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