Although the strong capacity of IL-18 in synergy with IL-12 to enhance Th1 type responses would be expected to down-regulated Th2 responses, high doses of IL-18 were reported to increase allergic sensitization, Th2 cytokine production and airway eosinophilia in a ragweed mouse model of allergic asthma, which was reversed in IFN-γ−/− mice [48]. This evidence concerns the gene IFNG and allergic asthma.