Skin barrier abnormalities have been shown to play an essential role in initiating early atopic dermatitis (AD). Antigen penetration via a compromised barrier may lead to heightened innate immune responses, antigen-presenting cell stimulation and priming of overt cutaneous disease. In a T_H2-promoting environment, T-cell/B-cell interactions in regional lymph nodes cause excessive IgE switch. Simultaneous redistribution of memory T cells into the circulation leads to exacerbation of AD through T-cell skin infiltration. Furthermore, it spreads beyond the skin to initiate the atopic march, including food allergy, asthma and allergic rhinitis. 

Primary interventions to prevent AD must focus on boosting skin barrier integrity, including supplementing barrier function with moisturizers. For secondary prophylaxis in children with established AD, we can stratify it into the prevention of disease exacerbations by using proactive approaches (with either topical corticosteroids or topical calcineurin inhibitors) in mild AD cases or the prevention of other atopic disorders that will likely mandate systemic immunosuppression in severe AD cases.

Source: Czarnowicki T, Krueger JG, Guttman-Yassky E. Novel concepts of prevention and treatment of atopic dermatitis through barrier and immune manipulations with implications for the atopic march. J Allergy Clin Immunol. 2017;139(6):1723-34.