Asthma is a disease characterized by symptoms, such as chronic airway inflammation, airway hyperresponsiveness (AHR) and mucus hypersecretion. Although steroids are the most effective anti-inflammatory therapy for asthma, they don‘t fully inhibit AHR and mucus production in a group of patients. IL-17A and IL-17F have been suggested to correlate with the severity of asthma, and we have previously shown the increased expression of IL-17A and MUC5AC, which did not respond to steroids, in house dust mite extract (HDM)-sensitized mice. In this study, we investigated the roles of these cytokines in both asthma pathogenesis and steroid sensitivity, using IL17A and IL17F-deficient mice (IL17A, IL-17F KO mice). Sensitization of HDM in IL17A, IL-17F KO mice markedly increased airway hypersensitivity and MUC5AC production compared to wild-type (WT) mice, whereas there was no change in inflammatory markers. In addition, dexamethasone attenuated inflammation, AHR and MUC5AC expression in IL17A, IL-17F KO mice, whereas it was not effective to MUC5AC expression in WT mice. These results suggest that IL-17A and IL-17F are involved in steroid-resistant mucus production. Though the mechanisms for this IL-17-induced steroid-resistance is being investigated, these data may provide new strategy to treat mucin in asthmatic patients.