脑出血的致死及致残率均高，但治疗手段匮乏。研究提示，神经血管单元（NVU）整体结构和功能的损伤可能是脑出血后继发性脑损伤的根本原因，小胶质细胞活化促发NVU持续损伤可能是这一瀑布级联反应的关键因素。CD200-CD200R1信号通路作为自身相关分子模式（SAMP），具有抑制小胶质细胞过度活化、保护血脑屏障、促进神经再生等多重作用。我们的前期研究发现，CD200-CD200R1信号通路可从多个方面调控损伤后反应，在加强组织损伤后“自我清除”和NVU稳态维持的同时规避了过度的免疫反应，而CD200-Fc可加强该调控作用。故此推断，脑出血后CD200-CD200R1信号通路很可能在小胶质细胞与NVU交互联系发挥桥梁作用。本研究拟通过细胞体系、动物模型及患者组织等多个层面，深入探究CD200-CD200R1信号通路在脑出血过程中的免疫调控作用和机制，并希望寻找脑出血继发性脑损伤的免疫治疗新靶点。

Intracerebral hemorrhage (ICH) is associated with high mortality and morbidity, while currently, no effective medical is available to improve functional outcomes in patients with ICH. Recently, studies revealed that cellular injury of ICH may be related to the neurovascular unit impairment, with microglia cells recognized as the key element in this context. CD200-CD200R signaling pathway has been proved to play crucial role in inhibiting the activation of microglia cells, suppressing release of inflammatory cytokines, protecting the BBB and promoting the neurogenesis. Our previous research also demonstrated that CD200-CD200R signaling pathway can modulate primary immune system in many aspects, especially elimination of apoptosis cells. Moreover, we also proved that this immune protection can enhanced by CD200-Fc. Therefore, we infer that CD200-CD200R signaling pathway probably modulate the crosstalk of microglia cells and NVU during ICH. Present study is designed to prove this hypothesis by in vitro and in vivo models, with multiple technologies, to investigate the immune modulatory mechanism CD200-CD200R conducted in ICH. These findings will help to find a new target of ICH treatment by interfering CD200-CD200R signaling pathway.