Abstract
Asthma is a common inflammatory disease of airways that is often associated with type 2 responses triggered by allergens, such as house dust mites (HDMs). IL-25 is a key mucosal cytokine that may be produced by stressed epithelial cells; it rapidly activates type 2 innate lymphoid cells to produce IL-13 and IL-5. When administered directly into lungs, IL-25 induces acute inflammation. However, the mechanisms underlying IL-25-initiated inflammation and the roles of this cytokine in the context of HDM-induced allergic inflammation are not fully understood. We show in this article that lung-resident conventional dendritic cells were direct targets of IL-25. IL-25-stimulated dendritic cells rapidly induced mediators, such as the chemokine CCL17, which, in turn, attracted IL-9-producing T cells. Importantly, these mechanisms also operated during HDM-induced allergic lung inflammation.