NKT cells are key actors at the interface between innate and acquired immunity. Indeed, upon activation by glycolipid antigens, they rapidly secrete both Th1 and Th2 cytokines, which affects the development of later immune responses. Previous studies have shown that NKT cells are essential for the development of allergic asthma, a prototypical Th2-mediated pathology. By contrast, three papers, two of which are published in this issue of the European Journal of Immunology, demonstrate, in mouse models, that treatment with alpha-galactosylceramide, a specific NKT ligand, inhibits most of the parameters associated with the disease, including airway hyperreactivity, eosinophilia and IgE production. Increased IFN-gamma synthesis, rather than regulatory IL-10, accounts for this paradoxical effect.