“…Accumulating evidence has shown that inflammatory responses of asthma are mediated by T-helper type 2 (Th2) cytokines including IL-4, IL-5, IL-9, and IL-13, which are critical for the synthesis of immunoglobulin IgE, the switch of T-helper cells toward the Th2 phenotype, and the survival of eosinophils 3. It has been suggested that alterations in cytokines network, including the overproduction of Th2 cytokines (interleukin [IL]-4, IL-5, and IL-13), the reduction in Th1 cytokines (interferon [IFN]-γ and IL-2), and abnormalities of IL-17, TGF-β, and thymic stromal lymphopoietin (TSLP), are involved in pathophysiology of asthma 4. A variety of innate immune cells, such as dendritic cells, mast cells, and epithelial cells, also contribute to the airway inflammation of asthma.…”