The cytokine IL-6 regulates the functions of CD4 T cells and mediates asthma induction, whereas IL-12 regulates the Th1/Th2 balance and promotes IFN-c production. IFN-c is related to the persistence and severity of asthma. IL-4 and IL-13, which are key cytokines in the pathogenesis of asthma, are involved in airway remodeling, inflammatory processes, airway hyperresponsiveness, goblet-cell hyperplasia, eosinophil infiltration, mucus hypersecretion, and B cell activation. IL-5 regulates the development, activation, migration, and survival of eosinophils, which are characteristic features of asthma. Asthma is controlled with bronchodilators, corticosteroids, leukotriene modifiers, theophylline, and/or anti-IgE therapy; however, none of these treatments are curative. These data can be further utilized to establish novel clinical diagnostic tools to enhance subsequent clinical application Inhaled corticosteroids are commonly used, but in addition to their side effects, these drugs tend to reduce glucocorticoid receptorbinding affinity and T-cell response. Therefore, alternative therapies are sought from traditional medicines or other natural products that have therapeutic effects in respiratory disorders. In our study, we found that ACA dose-dependently suppressed WBC infiltration of the lungs in mice with OVA-induced asthma, and 50 mg/kg/day ACA treatment reduced the WBC count to that of the vehicle control group. Specifically, eosinophil infiltration, which is characteristic of asthma, was significantly suppressed by ACA. In addition, ACA blocked OVA-induced histopathological changes such as airway remodeling, goblet-cell hyperplasia, eosinophil infiltration, and mucus plugs. Although treatment with ACA did not inhibit B cell activation, as assessed by CD79a expression, our results show that ACA is effective at reducing populations of CD4+ Th cells and CD8+ cytotoxic T cells in the lungs of mice with OVA-induced asthma. Finally, ACA downregulated Th2 cytokines IL-4 and IL-13 and Th1 cytokines IL-12a and IFN-c, but did not affect the secretion of IL-5. The relationship between Th1 cells and Th2 cells plays an important role in the pathogenesis of asthma. Mamessier and Magnan hypothesized that there are three situations related to asthma. In a healthy subject, activation of Th1 and Th2 cells is balanced, and the level of regulatory T-cell activation is relatively low. In well-controlled asthma, the level of Th1 cell activation is similar to that of regulatory T cells, but Th2 cell activation is suppressed. In uncontrolled asthma, the level of Th2 cell activation is lower than that of Th1 cells, which in turn is lower than that of regulatory T cells. Thus, not only is the balance between Th1 and Th2 cells important, equilibrium is needed between Th1/ Th2 cells and regulatory T cells. The Th2 cytokines IL-4 and IL-13 promote acute inflammatory processes in the pathogenesis of asthma and structural changes in the airways;. We found that ACA dose-dependently reduced IL-4 and IL-13 levels in the lungs. In addition, ACA decreased IL-12 a and INF-c levels as effectively as dexamethasone. Asthma was traditionally though to be initiated by an imbalance between Th1 and Th2 cells, The functions of IL-12 have been fairly well characterized; however, the role of INF-c in asthma has been controversial. Although Caenorhabditis elegans extract was reported to ameliorate asthma symptoms by increasing INF-c expression, hydrocortisone, which is used to treat asthma, has been shown to decrease INF-c expression. Previous studies have reported elevated INF-c levels in the BALF and bronchioles of asthma patients.