IL-17E, also known as IL-25, promotes Th2 biased immune responses. This is in contrast to other IL-17 family members which promote Th1 and Th17 biased inflammation. IL-17E is an important mediator of allergic reactions and protection against intestinal parasites. During helminth infections and allergic reactions, IL-17E production is locally upregulated in intestinal cells, airway epithelial cells, atopic dermatitis skin lesions, local Th2 cells, eosinophils, and basophils. It binds to IL-17RB but also requires IL-17RA to exert its activity. IL-17E acts on a variety of cell types which respond with increased production of Th2 cytokines and reduced production of Th1 and Th17 cytokines. Airway IL-17E can be activated by MMP7, a protease that is upregulated in airway epithelium in response to allergen exposure. Cleaved IL-17E shows enhanced binding to IL-17RB and stronger induction of Th2 cytokines. The Th2 cytokines, in turn, trigger the expansion of Th2 memory cells and anti-inflammatory M2 macrophages, increased eosinophil mobilization and activation, and dendritic cell migration. These actions promote protective anti-helminth immune responses as well as allergic inflammation and airway hyperreactivity. IL-17E also promotes vascular endothelial cell proliferation and assembly into tubular structures. It also supports the integrity of the blood brain barrier and limits CD4+ T cell infiltration into the brain.