Cerebral ischemia-reperfusion injury induces a secondary immune inflammatory reaction that exacerbates brain injury and clinical prognosis. Dendritic cells (DCs) and microglia are both important regulators of neuroinflammation. Studies have confirmed that a large number of cells express the DC surface marker CD11c in the ischemic area, and some of these cells also express microglial markers. However, the specific mechanism of transformation between microglia and DCs and their roles in the process of cerebral ischemia-reperfusion injury are still not clear. In this study, we established a mouse model and flow cytometry was used to detect the expression of mature DC surface molecules in activated microglia. IFN-γ knockout mice were used to determine the regulatory effect of IFN-γ on microglial transformation. We found that CD11c⁺ cells were derived from microglia after ischemia-reperfusion injury, and this group of cells highly expressed MHC-II molecules and other costimulatory molecules, such as CD80 and CD86, which were regulated by IFN-γ and its downstream signaling molecules ERK/c-myc. In summary, our results showed in cerebral ischemia-reperfusion injury, IFN-γ regulates the transformation of microglia to DC-like cells. Microglial-derived DC-like cells possess the ability to present antigens and activate naïve T cells which is regulated by the ERK/c-myc signaling pathway.

脑缺血再灌注损伤诱发继发性免疫炎症反应，加剧脑损伤和临床预后。树突状细胞 (DC) 和小胶质细胞都是神经炎症的重要调节剂。研究证实，大量细胞在缺血区表达DC表面标志物CD11c，其中一些细胞还表达小胶质细胞标志物。然而，小胶质细胞与DCs转化的具体机制及其在脑缺血再灌注损伤过程中的作用尚不清楚。在本研究中，我们建立了小鼠模型，并使用流式细胞术检测活化小胶质细胞中成熟 DC 表面分子的表达。使用 IFN-γ 敲除小鼠来确定 IFN-γ 对小胶质细胞转化的调节作用。我们发现 CD11c⁺细胞来源于缺血再灌注损伤后的小胶质细胞，该组细胞高表达 MHC-II 分子和其他共刺激分子，如 CD80 和 CD86，受 IFN-γ 及其下游信号分子 ERK/c-我的C。总之，我们的结果表明，在脑缺血再灌注损伤中，IFN-γ 调节小胶质细胞向 DC 样细胞的转化。小胶质细胞衍生的 DC 样细胞具有呈递抗原和激活受 ERK/c-myc 信号通路调节的幼稚 T 细胞的能力。