Shared epigenetic mechanisms in atopic dermatitis and food allergy: a review of immune dysregulation at the skin-gut axis.

Atopic dermatitis and food allergy frequently coexist and are central features of the atopic march, which describes the progression from eczema to allergic rhinitis and asthma. Classical genetic factors, such as FLG mutations, account for only a partial contribution to disease susceptibility. Recent research highlights epigenetic regulation, including DNA methylation, histone modification and noncoding RNAs, as pivotal determinants of immune dysregulation and barrier dysfunction. This review systematically examines shared epigenetic signatures between atopic dermatitis and food allergy, with particular emphasis on the interleukin (IL)-4/IL-13 axis, FOXP3 methylation and epithelial gene silencing at the skin-gut interface. By integrating evidence from genome-wide methylation and transcriptomic studies, it is proposed that epigenetic plasticity underlies the immune barrier crosstalk that drives atopic comorbidity. Elucidating these mechanisms provides a foundation for biomarker discovery and the development of personalized epigenetic therapies in allergy and dermatology.