胶质瘤治疗是当今医学界亟需解决的难题。文献报道，炎症应答诱导免疫系统杀伤胶质瘤细胞是重要的治疗手段。CD100阳性NK细胞（NKCCD100+）是黏附性最强的NKC亚群之一，既参与炎症免疫应答，又拮抗肿瘤，但分子机制尚不清楚。我们前期研究发现，发生颅内感染的胶质瘤患者脑脊液中，NKCCD100+亚群数量最多，患者远期肿瘤复发率显著降低。进一步发现，NKCCD100+黏附于胶质瘤细胞上，上调其受体Plexin-B1，进而调控肿瘤相关分子Survivin和MMP9表达，强烈提示NKCCD100+在抑制胶质瘤增殖和侵袭中发挥重要作用。本课题拟搞清NKCCD100+亚群等在患者脑脊液中的表达规律。深入探讨并明确NKCCD100+调控胶质瘤细胞Plexin-B1-Survivin/MMP9信号通路,进而影响胶质瘤细胞侵袭和转归的功能特点和分子机制，为临床应用炎症应答治疗胶质瘤提供新的理论和实验依据。

Glioma is the common type of intracranial malignant tumor. Inflamation induced-cytotoxicity to tumor cell is one of the new strategy for glioma immunotherapy. CD100 positive natural killer (NK) cells are one of the effector lymphocytes of the innate immune system bearing strong adhension effect that control several types of tumors and microbial infections. Previously, we found that CD100 positive NK cells were the major lymphocytes appearing in the cerebrospinal fluid from glioma patients undergoing the intracranial infection after the operation. Meanwhile, the soluble form of CD100 (sCD100) were greatly increased in the cerebrospinal fluid, and the recurrence of glioma in 15 months of patients were greatly reduced .Further studies showed that Plexin-B1, receptor for CD100, expressed on glioma cells was upregulated when binding with CD100+ NK cells during the intracranial inflammation, and regulated the expression of Survivin and MMP9, which involved in the apoptosis and invasion of glioma cells. However, the mechanisms underlying the anti-glioma effect of this subset is still unknown. In the present study, we will first detect the roles of CD100 expression on NK cells and sCD100 during the the intracranial inflammation after the operation in glioma patients. Then we will establish coculture systems containing both NK cells and glioma cells, and modle of NOD/SCID mice bearing glioma .After that we will detect the molecular mechanisms of CD100 positive NK cell in regulation of molecules involved in Plexin-B1-Survivin/MMP9 pathway on the apoptosis and invasion of glioma cells both in vitro and in vivo. This study may declare the mechanisms of CD100 positive NK cells to glioma cells during the intracranial inflamation after the craniocerebral operation and provide the new experimental basis to improve the success of glioma immunotherapy.