Allergens and infections with parasitic helminths preferentially induce Th2 immune responses associated with elevated levels of serum immunoglobulin E (IgE) and expansion of eosinophils and mast cells. Interleukin-4 (IL-4) is a key cytokine in the differentiation of naive CD4⁺ T cells into Th2 cells, which produce a panel of cytokines including IL-4, IL-5, IL-6, IL-9, IL-10, and IL-13 [1] and have been shown to trigger recovery from gastrointestinal nematodes [2]. Nonetheless, mice deficient for IL-4 have been shown to develop residual Th2 responses [3–5] and can expel the nematode Nippostrongylus brasiliensis[6], suggesting that there is a functional equivalent of IL-4 in these processes. IL-13 is a cytokine that shares some, but not all, biological activities with IL-4 [7,8]. There is now compelling evidence that IL-4 and IL-13 share receptor components, including IL-4Rα and IL-13Rα1 [9]. In order to dissect the roles of IL-4 and IL-13 in the regulation of Th2 cells and in the response to nematode infections, we looked for differences between mice deficient for either the IL-4 gene or the IL-4Rα gene. Unlike IL-4, IL-4Rα was required for control of N. brasiliensis, and Th2 development during infection – as characterized by cytokine production, GATA-3 and surface CD30 expression – was more severely affected in IL-4Rα^−/− mice than in IL-4^−/− mice. Injection of recombinant IL-13 induced worm expulsion in otherwise incompetent RAG2^−/− mice. Our results suggest that IL-13 regulates Th2 responses to nematode infection and requires IL-4Rα.