Atopic dermatitis (AD) is an allergic skin disease with a genetic predisposition. The pathogenesis is complex, including environment stimulation, epidermal barrier deficiency, and autoimmune disorders. The destruction of epidermal barrier stimulates the inflammatory response. In acute period, Th2 cells are activated to produce IL-4 and induce B lymphocytes to secrete IgE. Thus leads to degranulation of mast cells and basophils. After acute period, epidermis is thickened, accompanied with increasing expression levels of several chemokines and cytokines. In chronic phase, the cellular infiltration includes mainly Th1 and Th2 cells, and less Th17 and Th22 cells. The latter two cells together with their specific cytokines and chemokines are derived from keratinocytes and fibroblasts, which can produce tissue remodeling and fibrosis. So far, the treatment of AD contains allergens exposure avoid, anti-inflammatory, anti-infection, phototherapy, and immune therapy, etc.

Dermatitis, atopic/ET/TH; Editorial