中文摘要：

目的研究抑制树突状细胞（DCs）自噬对DCs功能及小鼠哮喘的影响。方法 （1）将BALB/c小鼠按随机数字表法分为3组：急性哮喘对照组（哮喘组）、哮喘自噬抑制剂氯喹（CQ）治疗组（CQ组）和空白对照组（对照组）。哮喘组和CQ组利用卵清蛋白（OVA）诱导建立小鼠过敏性哮喘模型,CQ组加用CQ。用H-E染色观察各组小鼠肺组织的病理改变,酶联免疫吸附实验、蛋白质印迹实验、流式细胞术分别检测各组小鼠血清OVA特异性IgE以及肺DCs自噬水平、表面共刺激分子和主要组织相容性复合体Ⅱ类分子（MHCⅡ）的表达水平。（2）体外用自噬抑制剂3-甲基腺嘌呤（3MA）抑制C57/B6小鼠骨髓源DCs自噬,检测DCs表面共刺激分子、MHCⅡ的表达水平。（3）获取OT2小鼠脾脏CD4＋T淋巴细胞,与各组肺DCs以1∶10的比例混匀,流式细胞术检测T细胞的增殖情况与活化反应。结果 （1）CQ组IgE的表达水平（P〈0.05）、肺炎症细胞浸润程度以及肺DCs自噬水平（P〈0.05）和CD86、MHCⅡ表达水平（P〈0.05）均低于哮喘组。（2）3MA体外抑制骨髓源DCs自噬后,DCs表面的CD86及MHCⅡ表达均低于哮喘组（P〈0.05）。（3）CQ组肺DCs体外诱导的T细胞增殖能力与活化反应均弱于哮喘组（P〈0.05）。结论自噬抑制剂可抑制过敏性哮喘肺DCs的自噬,下调DCs表面共刺激分子、MHCⅡ的表达以及DCs诱导的T细胞增殖能力,改善哮喘病情。

英文摘要：

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 MHC Ⅱ （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 MHC Ⅱ 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 su