免疫抑制微环境和血管新生与胶质瘤的进展高度相关。前期研究结果发现：DNA结合抑制因子ID2是KDR上游关键调控分子，抑制ID2在MDSC中的表达可以影响骨髓源性细胞分化，并延缓小鼠胶质瘤的生长。据此提出ID2介导的MDSC是促胶质瘤进展的重要因素的假说。本项目拟检测临床、小鼠胶质瘤样本（血液和组织）中ID2表达以及骨髓源性细胞分化状态、比例与胶质瘤进展级别、预后的关系。以ID2-/-和ID2+/+ MDSC与胶质瘤细胞共培养体系、胶质瘤PDX模型以及RCAS-TVA PDGF或P53小鼠胶质瘤/复发模型为研究对象，运用MDSC细胞移植、流式细胞术、小动物CT等观察ID2介导的MDSC分化及对胶质瘤进展的作用，并通过免疫印迹、免疫组化、高通量测序等手段，探索ID2介导MDSC干预胶质瘤进展的机制及相关基因表达，以证明该假说，为胶质瘤的免疫干预治疗及新型特异分子靶向细胞治疗提供新策略和思路。

Immunosuppressive microenvironments and angiogenesis are highly correlated with the progression of gliomas. The applicant's preliminary studies found that: ID2 is a key upstream regulator of KDR molecule, inhibition of ID2 expression in BMDC can affect bone marrow-derived cell differentiation, and delay the growth of glioma in mice. In view of this, the hypothesis that ID2-mediated MDSC is an important factor in the progression of glioma has been proposed. This project intends to detect clinical and mouse glioma ID2 expression and bone marrow-derived cell differentiation status in blood and tissue, with the progression and prognosis of glioma. Using ID2 -/- and ID2 +/+ MDSC and glioma cells Co-culture system, glioma PDX model and RCAS-TVA PDGF or P53 mouse glioma / relapse model as the research object, using MDSC cell transplantation, flow cytometry, small animal CT observed ID2-mediated MDSC differentiation and its effect on the progress of glioma, and further explore the mechanism of ID2-mediated MDSC intervention in glioma progression and related gene expression by means of immunoblot, immunohistochemistry, high-throughput sequencing to prove the hypothesis, all of which will provide some new ideas and strategies for the immune intervention and molecular targeted cell therapy of glioma in the future.