In the fungi-induced allergic airway inflammation, IL-22 is indispensably required, IL-22 absence attenuates proallergic and proinflammatory responses, and neutralization of IL-22 improves lung function [23]; in addition, in epicutaneous-sensitized and OVA-induced allergic airway inflammation, the generation of CD4+ T cells producing IL-22 is promoted, meanwhile, promoting the production of IL-17A and exacerbating airway inflammation and AHR [24]. The gene discussed is IL17A; the disease is inflammatory response.