IL25 and asthma: While overexpression of IL-17E in the lung resulted in significantly enhanced antigen-induced Th2 cell infiltration and T2 type cytokine production, pronounced airway eosinophilia, goblet cell hyperplasia in the airways, and airway remodeling, neutralization of this cytokine either by application of a soluble IL-17E receptor or by an anti-IL-17E-antibody lowered allergic airway inflammation and pathological features of experimental asthma in mice [88,89].