As the first cell barrier to outer allergens, the airway epithelial cells showed a decreased wound repair and anti-oxidation ability after ITGB4 was downregulated. ITGB4 is an important adhesion molecule that mediates the anchoring of airway epithelial cells to the basal membrane. Given that ITGB4 is known to engage in multiple signaling pathways that may influence many physiological functions of airway epithelial cells, we questioned whether downregulation of ITGB4 enhanced the invasion of inhaled allergens and regulated the local T cell Panaxadiol immune inflammation through antigen presentation process. In this study, ITGB4 was silenced by a specific siRNA virus vector. We observed that downregulation of ITGB4 is associated with blocked antigen presentation ability, decreased MHC class II expression and altered B7 homologs expression on airway epithelial cells. Furthermore, decreased T cell proliferation and differential cytokine production was induced after co-culturing with ITGB4-silenced epithelial cells. Allergy immune disorder diseases like asthma are characterized by Th2-mediated inflammation and structural disruption of airway epithelia cells. In these diseases, an increase in Th2 cell infiltration and Th2 cytokine expression is induced after allergy exposure. However, the intrinsic molecular mechanism underlying this Th2 inflammation bias is not fully understood. Previous studies demonstrate that airway epithelial cells engage in the initiation and regulation of inflammation and immune responses through production of cytokines and RS-127445 chemokines and others. Recent studies further showed that bronchial epithelial cells are capable of antigen presentation and thus can regulate the local airway immune cells and inflammation reactions. Especially, T cells can be effectively activated by airway epithelial cells through antigen presentation after allergen exposure on the airway. The airway epithelial barrier is often disrupted in asthma patients, with evidence for shedding of airway epithelial cells and disparity expression of genes. Our previous study demonstrated that ITGB4 is downregulated in asthma airway epithelial cells, which may result in decreased wound repair and anti-oxidation ability. In this current study, our results demonstrated for the first time that downregulation of ITGB4 blocked the process of antigen trafficking which indicated that the ITGB4-silenced cells are damaged cells and cannot maintain the normal function of monitoring outer allergens and present the foreign antigen to local T cells. As effective APCs, the recognition and uptake of outside allergens is the first step for the local immune homeostasis. Furthermore, the uptake and presentation of antigen by APCs has a close relationship to the activation and differentiation of local T cells. Therefore, we examined the influence of ITGB4 silencing on local airway T cells inflammation. By CFSE staining and BrdU-incorporation assay, we found that the proliferation of T cells was inhibited after coculturing with ITGB4-silenced 16HBE14o- cells. At the same time, T cell-derived IFN-gamma was reduced; IL-17 was increased by ELISA detection and intercellular cytokine staining. It is well known that Th2 cells orchestrate allergy-induced asthmatic inflammatory responses, and the main immune abnormalities are caused by Th2 cytokines, such as IL-4 and IL-5, which induce eosinophil infiltration and airway hyperresponsiveness. On the contrary, IFN-gamma, a Th1 cytokine, reduces airway inflammation and airway hyperesponsiveness in asthma models and clinical traits.