Mice deficient in CD1d-/- and Jα18-/- iNKT cells showed a decrease in airway hyperresponsiveness and eosinophilia, while the adoptive transfer of IL-4- and IL-13-producing iNKT cells restored the airway inflammation (38, 39), suggesting that type 2 iNKT cells are responsible for asthmatic inflammation (20, 40). Here, IL4 is linked to airway hyperresponsiveness.