很大一部分肿瘤患者因手术、放化疗和凝血紊乱等因素在短期内并发脑卒中。回顾性临床研究提示肿瘤患者发生缺血性脑卒中后死亡率高、生存期短，但是缺乏理论基础和机制研究。在前期研究中，我们应用皮下荷瘤小鼠建立脑卒中模型，发现卒中后梗死体积明显大于非荷瘤小鼠，但机制不明。调节性T细胞(Treg)是脑卒中后抑制神经炎症的内源性保护因素，而在肿瘤状态下Treg可介导肿瘤细胞的免疫逃逸。预实验提示脑卒中使Treg表面的膜受体Neurophilin-1(Nrp1)表达增高，而肿瘤合并脑卒中时，Treg向肿瘤组织的趋化明显增强，由此我们提出假说：肿瘤小鼠发生的缺血性脑卒中加重了Treg在Nrp1的作用下向肿瘤募集，减少了Treg向缺血脑区的趋化，从而导致肿瘤合并脑卒中状态下脑损伤的加重。本研究拟应用小动物活体荧光成像和Nrp1条件敲除小鼠等技术证明上述假说，为肿瘤合并脑卒中患者的治疗提供新的靶点和理论依据。

Cancer patients have a high possibility of stroke comorbidity due to adverse events related to treatments and cancer induced coagulation disturbances etc. Retrospective clinical studies indicated that ischemic stroke injuries in cancer patients were severe mainly reflected by high mortality and short survival period. However, the theoretical basis has not been reported. We demonstrated that pre-existing cancer exacerbated infarct volume growth after stroke using a distal middle cerebral artery occlusion model in mice with subcutaneous tumor. The mechanisms remain unclear. Regulatory T cell (Treg) is an endogenous protective factor that inhibits neurological inflammation after stroke, while mediates immune escape of tumor cell. Our results indicated that stroke increased the expression of neurophilin-1 (Nrp1) on the surface of Treg, and enhanced the chemotaxis of Treg to tumor tissue in mice with pre-existing cancer. Therefore, we put forward the hypothesis that ischemic stroke in mice with pre-existing colon cancer augments peripheral Treg cells infiltration into the tumor but hinders Tregs’ recruitment into the brain, further increases ischemic brain damage. In this study, the main aim is to prove the above hypothesis using the techniques of in vivo fluorescence imaging and Nrp1 knockout mice. Our study can provide a theoretical basis for the treatment of cancer patients complicated by stroke.