Objective To study the impact of autophagy inhibition on functions of dendritic cells (DCs) and mouse model of allergic asthma. Methods (1)BALB/c mice were divided into three groups using the random number table: asthma model group, asthma treated with autophagy inhibitor (chloroquine) group (asthma+CQ group) and control group. Mouse models in asthma group and asthma+CQ group were induced with ovalbumin (OVA); meanwhile, mice of asthma+CQ group were also treated with autophagy inhibitor CQ. Hematoxylin-Eosin (H-E) staining was used to observe the pathological changes in lung tissues of mice. ELISA, Western blotting analysis and flow cytometery were used to detect the serum OVA-specific IgE, autophagy level, and expression of surface co-stimulatory molecules and major histocompatibility complex class Ⅱ(MHC Ⅱ) on lung DCs, respectively. (2)Bone marrow-derived DCs were treated with autophagy inhibitor 3-methyladenine (3MA) in vitro and the surface expression of co-stimulatory molecules and MHC Ⅱ was detected. (3) We sorted CD4⁺ T cells from spleens of OT2 mice, then co-cultured with lung DCs from mice of different groups (T cells:DCs=1:10), and detected the activation and proliferation of T cells with flow cytometery. Results (1) The level of OVA-specific IgE (P<0.05), extent of inflammatory cell infiltration in lung tissues, autophagy level in lung DCs (P<0.05), and expression of CD86 and MHCⅡ (P<0.05)on lung DCs in asthma+CQ group were significantly lower than those in the asthma group. (2) 3-MA treatment decreased the surface expression of CD86 and MHCⅡ on bone marrow-derived DCs (P<0.05). And (3) lung DCs from asthma+CQ group had lower ability for activating T cells and promoting T cell proliferation than those from the asthma group (P<0.05). Conclusion Autophagy inhibitors can improve the pathologic condition of allergic asthma through inhibiting autophagy in DCs, down-regulating surface expression of co-stimulatory molecules and MHCⅡon DCs, and further inhibiting the DCs-induced proliferation of T cells.