Epidermal barrier defects and immune abnormalities are the main pathophysiological changes in the development of atopic dermatitis (AD) . Skin keratinocytes can release a variety of inflammatory factors and mediators under the treatment with various harmful factors. Three epithelium-derived cytokines interleukin (IL) -33, IL-25 and thymic stromal lymphopoietin are considered to be effective inducers of Th2 immune response in skin or mucosal barrier, which can activate immune cells, cause the secretion of Th2 cytokines, enhance the Th2 immune response, and participate in the occurrence and development of AD. This review focuses on the role of the above 3 epithelium-derived cytokines in the pathogenesis of AD.

Janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling pathway plays an important role in immune pathways in atopic dermatitis (AD) . Drugs that block the JAK-STAT signaling pathway, such as classic JAK inhibitors tofacitinib, ruxolitinib, etc., have been gradually applied to the treatment of AD in clinical trials, and good clinical efficacy has been achieved. In addition, other inhibitors of the JAK-STAT signaling pathway, such as apamin and dupilumab, also show some efficacy in the treatment of AD. This review summarizes recent studies on the JAK-STAT signaling pathway and its inhibitors.