Allergic inflammation and infection with helminths often elicit a strong type 2 immune response characterized by increased numbers of IL-4/IL-13 producing cells of the innate and adaptive immune sytem. Using conditional IL-4/IL-13-deficient mice and mixed bone marrow chimeras we investigated the contribution of different IL-4/IL-13-producing cell types for type 2 immune responses in vivo. We observed that expression of IL-4 by T cells outside the B cell follicle was sufficient to induce GC formation and efficient IgE and IgG1 switching in the context of a type 2 immune response. Further, T cell-derived IL-4/IL-13 was required for alum/OVA-induced accumulation of ILC2s and allergic inflammation of the lung but dispensable for elimination of gastrointestinal helminths. Basophils played an important role for IgE-mediated allergic skin inflammation and protective immunity against secondary helminth infections which required IgE-elicited release of IL-4/IL-13 from basophils. To further investigate the IL-4/IL-13-elicited effector pathways in vivo, we generated mice which express a Cre-inducible and constitutively active version of STAT6. Crossing these mice to VillinCre mice resulted in spontaneous goblet cell hyperplasia and increased numbers of tuft cells in the intestinal epithelium. Expression of activated STAT6 in intestinal epithelial cells was sufficient for worm expulsion in the absence of CD4 T cells.