Background: IL-23 has been postulated to be a critical mediator contributing to various inflammatory diseases. Dermatophagoides pteronyssinus (Der p) is one of the most common inhalant allergens. However, the role of IL-23 in Der p-induced mouse asthma model is not well understood, particularly with regard to the development of allergic sensitization in the airways. Objective: To evaluate roles of IL-23 in Der p-sensitization and asthma development. Methods: BALB/c mice were repeatedly administered with Der p intra-nasally to develop Der p-allergic sensitization and asthma. After Der p local administration, changes in IL-23 expression were examined in lung tissues and primary epithelial cells. Anti-IL-23p19 antibody was given during the Der p sensitization period, and its effects were examined. Effects of anti-IL-23p19 antibody at bronchial epithelial levels were also examined in vitro. Results: The expression of IL-23 at bronchial epithelial layers was increased after Der p local administration in mouse. In Der p-induced mouse models, anti-IL-23p19 antibody treatment during allergen sensitization significantly diminished Der p-allergic sensitization and several features of allergic asthma including the production of Th2 cytokines and the population of ILC2 in lungs. The activation of dendritic cells in lung-draining lymph nodes was also reduced by anti-IL-23 treatment. In MLE-12 cells, IL-23 blockade prevented cytokine responses to Der p stimulation, such as IL-1α, GM-CSF, IL-33, and also bone marrow-derived DCs activation. Conclusion: IL-23 is another important bronchial epithelial cell-driven cytokine which may contribute to the development of house dust mite allergic sensitization and asthma.