FIGURE 1.

Main pathogenesis and mechanisms of AD. Epidermal barrier disruption mainly caused by mechanical scratch and aberrant inflammatory reactions. Reduced FLG contributes to inflammatory changes, while the releasing proinflammatory cytokines and chemokines result in further FLG deficiency. It is a positive feedback loop. LC and DC recognize the allergens and microbial components and stimulate adaptive immune responses—predominantly T_H2/T_H22 bias in the acute phase and T_H1/T_H17 bias in the chronic phase. The release of alarmins (including IL-10, IL-31, and TSLP) from epithelial cells promotes ILC2 induction as an innate immune response and aggravates T_H2 immune response. T_H2 cytokines IL-4, IL-5, and IL-13 recruit eosinophils and increase B cell IgE production during the acute phase. IL-22, produced by T_H22, promotes T_H2-type inflammation. In the chronic stage, T_H1 and cytokines predominate in skin lesions, leading to further inflammation and epidermal hyperplasia. Inflammatory cytokines simultaneously impair the skin barrier by inhibiting barrier proteins and disrupting skin microbiota, thereby increasing the risk of S. aureus colonization.