Interleukin‐18 (IL‐18) has been regarded as a proinflammatory cytokine because of its potent interferon‐γ‐inducing activity. However, mutant mice that release excess amounts of IL‐18 spontaneously develop pruritic chronic dermatitis‐like atopic dermatitis (AD), suggesting the importance of IL‐18 for the development of AD. Intriguingly, depletion of il‐18 but not stat6, an essential transcriptional factor for IL‐4 signaling, rescues the mice from AD, indicating IL‐18‐dependent, T‐helper 2 (Th2) cell‐independent AD. This type of AD is classified as innate‐type allergy in contrast to Th2 cell‐dependent ordinary allergy. Consistent with the previous studies, mice transferred with antigen‐specific Th1 cells exhibit no airway hyperresponsiveness and respiratory eosinophilic inflammation after challenge with antigen alone. However, they suffer from asthma upon challenge with antigen plus IL‐18, with comparable levels of both the alterations as in those transferred with Th2 cells following challenge with antigen. The former type of asthma is categorized as Th1‐associated allergy. Therefore, it is definitely necessary to evaluate whether individual allergic disorders involve either of these IL‐18‐mediated pathways or a Th2‐mediated one.