Mechanisms of allergic inflammation in asthma. Epithelial cell activation by allergens, viruses, bacteria and pollutants takes place and their proinflammatory cytokines and chemokines induce inflammation and contribute to Th2 response with TNF-α, IL-13, TSLP, IL-31, IL-33. Th2 response involves multiple cytokines such as IL-4, IL-5, IL-9, IL-13, IL-25, IL-33, eosinophilia, and local and systemic IgE production. A series of chemokines are produced and migration of inflammatory cells to the allergic tissues takes place. In addition, other effector T cell subsets, such as Th9, Th17 and Th22 cells play inflammatory roles. Cross-linking of IgE receptor FcεRI on the surface of mast cells and basophils and their degranulation, induces a type 1 allergic response. The activation of smooth muscle cells, myofibroblasts, angiogenesis and subepithelial fibrosis, lead to remodeling. Bronchial hyperreactivity takes place, with enhanced susceptibility to bronchoconstriction. Innate lymphoid cells may contribute to many aspects of allergic inflammation by the help of multiple cytokines. Epithelial apoptosis and shedding are essential in the mechanisms of eczema and asthma [23, 24]. Survival and reactivation of migrating inflammatory cells and their interaction with resident tissue cells and other inflammatory cells augment allergic inflammation.