Asthma is defined by a chronic airway inflammatory disease, characterized by wide variation over short periods of time in resistance to flow in the airways of the lung. It is well known that IL -13 is a central mediator of allergic asthma and lung specific IL-13 transgenic (TG) (+) mice demonstrated airway inflammation characterized by macrophage and eosinophil infiltrations and airway remodeling, such as subepithelial fibrosis. Lung specific IFN-g TG (+) mice have been well known to have enhanced airway inflammation characterized by macrophage, lymphocyte, and neutrophil infiltrations. Interestingly, these TG mice have markedly enhanced airways hyperresponsiveness (AHR) on methacholine challenge. Moreover, IFN-g mRNA expression was markedly enhanced in induced sputum from severe asthmatics when compared with mild ones, suggesting that IFN-g is an important mediator on the progression to severe asthma. Taken together, these findings suggest that IFN-g which is secreted from Th1 cells as well as IL-13 are important mediators for the immunopathogenesis of asthma. From this hypothesis this review describes the importance of innate immunity for the development of asthma.