Atopic dermatitis (AD) is a common skin disorder, characterized by a complex and heterogeneous pathogenesis that includes skin barrier dysfunction, allergy/immunology, and pruritus. For example, when the skin barrier is disrupted by mutations in the filaggrin gene or by environmental factors, the skin becomes more susceptible to external stimuli. Exposure to protein antigens induces a Th2-dominant state via mediators such as thymic stromal lymphopoietin (TSLP); the Th2 cytokines IL-4 and IL-13 induce IgE class switch. More recently, it has been shown that Th2 cells produce IL-31, which induces pruritus, and that Th2 cytokines reduce filaggrin expression by keratinocytes. These findings suggest that the Th2 environment causes IgE induction, pruritus, and barrier dysfunction.