人脑胶质瘤是中枢神经系统最常见的恶性肿瘤，传统疗法效果差。虽然多种免疫治疗策略相继问世，但在临床试验中鲜有成效，其微环境中浸润的肿瘤相关巨噬细胞（TAMs）等被认为是影响疗效的重要因素。胶质瘤相关外泌体调控途径为研究胶质瘤细胞与微环境中TAMs等免疫细胞间细胞通讯和极化调控提供了新思路。我们发现低氧诱导的胶质瘤外泌体能够显著上调TAMs的自噬水平，进而促进其M2极化，且低氧胶质瘤外泌体中整体转运的IL-6/IL-6R/MIR-155-3p通路在此过程中起关键作用。本课题拟通过表达谱芯片与生物信息学预测相结合，在体外和体内全面筛选并验证MIR-155-3p促TAMs自噬及极化的关键靶基因，阐明胶质瘤外泌体相关“IL-6/IL-6R/MIR-155-3p/自噬”通路整体转运假说，及其促进TAMs免疫抑制能力的分子机制，并针对关键节点设计干预方案，为改善现有胶质瘤免疫治疗策略提供新的理论依据。

As the most common malignant primary brain tumor, glioblastoma multiforme (GBM) responds poorly to conventional treatment. Although novel immunotherapies have been applied into glioma treatment, the prognosis of glioma patients is still very bad. Immunosuppressive microenvironment of glioma, which contains the tumor-associated macrophages (TAMs) plays important roles in the resistance to the treatments of this cancer. The regulating function of glioma-derived exosome on immune cells intrigued us to find new ideas in investigating the interactions between glioma cells and immune cells like TAMs. We have found that hypoxia induced Glioma-Derived Exosomes can significantly promote the expansion and M2 polarization of TAMs and that the integral-transfer of IL-6/MIR-155 pathway within hypoxia induced glioma-derived-exosomes plays the important roles during this process. We aim to provide new theoretical basis for modifying the current glioma immuno-therapy by interfering the TAMs autophagy and polarization.More importantly, we plan to interfere the critical TAMs autophagy and polarization associated molecules to provide new theoretical basis for modifying the current glioma immunotherapy.