It has been well-established that type-2 immunity, characterized by eosinophilia, goblet cell hyperplasia, mucus production, and B cell class switching to IgE, is highly dependent on the production of the type-2 cytokines, interleukin (IL)-4, IL-5, IL-9, and IL-13, by T helper 2 (Th2) cells. However, it is less clear how the type-2 cytokine effector response is induced and in addition what innate cell type produces the initiating factor. Recent reports highlight IL-25 as a type-2 inducing factor, with IL-25 administration resulting in severe gut and lung type-2 pathologies. The expression of IL-25 is also necessary for initiation of a robust type-2 response both at the genesis of the response, as with helminth infection, and during the response, as has been shown in experimental allergic asthma. It is also apparent that, as well as directly controlling type-2 immunity via IL-4, IL-5, and IL-13, IL-25 may also interact with other cytokines and their receptors, such as IL-17A and the IL-17RA receptor. Here, we review the role of IL-25 as an important factor in controlling the initiation and severity of the type-2 response, and as an alternative therapeutic target to the type-2 cytokine family, for the treatment of allergic asthma. (c) 2009 International Union of Biochemistry and Molecular Biology, Inc.