Abstract
The role of epigenetic processes, primarily DNA methylation, in allergic disease susceptibility and severity is actively explored because of the inability of genetic factors to explain more than a small proportion of the variance in disease phenotype and the functional link among epigenetic mechanisms, environmental exposures, and developmental programs. To date, a number of genome-wide and candidate-gene DNA methylation studies have been performed in populations with asthma, allergic rhinitis, or atopic dermatitis, focusing not only on peripheral blood but also on airway tissue and lesional skin. Differential DNA methylation was detected at biologically plausible loci, but these initial studies should be considered exploratory because of potential issues with population design, size, and phenotypic heterogeneity. Studies leveraging DNA methylation data as clinical biomarkers are also beginning. Future work in longitudinal mother–child birth cohorts will likely highlight the contribution that methylome screens can give to the clinical management of allergic disease and unveil the role played by epigenetic mechanisms in allergic disease pathogenesis.
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