Ischemic stroke, which accounts for 75–80% of all strokes, is the predominant cause of morbidity and mortality worldwide. The post-stroke immune response has recently emerged as a new breakthrough target in the treatment strategy for ischemic stroke. Glial cells, including microglia, astrocytes, and oligodendrocytes, are the primary components of the peri-infarct environment in the central nervous system (CNS) and have been implicated in post-stroke immune regulation. However, increasing evidence suggests that glial cells exert beneficial and detrimental effects during ischemic stroke. Microglia, which survey CNS homeostasis and regulate innate immune responses, are rapidly activated after ischemic stroke. Activated microglia release inflammatory cytokines that induce neuronal tissue injury. By contrast, anti-inflammatory cytokines and neurotrophic factors secreted by alternatively activated microglia are beneficial for recovery after ischemic stroke. Astrocyte activation and reactive gliosis in ischemic stroke contribute to limiting brain injury and re-establishing CNS homeostasis. However, glial scarring hinders neuronal reconnection and extension. Neuroinflammation affects the demyelination and remyelination of oligodendrocytes. Myelin-associated antigens released from oligodendrocytes activate peripheral T cells, thereby resulting in the autoimmune response. Oligodendrocyte precursor cells, which can differentiate into oligodendrocytes, follow an ischemic stroke and may result in functional recovery. Herein, we discuss the mechanisms of post-stroke immune regulation mediated by glial cells and the interaction between glial cells and neurons. In addition, we describe the potential roles of various glial cells at different stages of ischemic stroke and discuss future intervention targets.

缺血性中风占所有中风的75-80％，是全世界发病率和死亡率的主要原因。最近，中风后免疫应答已成为缺血性中风治疗策略中的新突破目标。胶质细胞，包括小胶质细胞，星形胶质细胞和少突胶质细胞，是中枢神经系统（CNS）梗塞周围环境的主要组成部分，与中风后免疫调节有关。然而，越来越多的证据表明神经胶质细胞在缺血性中风中发挥有益和有害的作用。调查神经中枢神经系统稳态并调节先天免疫反应的小胶质细胞在缺血性中风后迅速激活。活化的小胶质细胞释放诱导神经元组织损伤的炎性细胞因子。相比之下，交替激活的小胶质细胞分泌的抗炎细胞因子和神经营养因子有助于缺血性中风后的恢复。缺血性中风中的星形胶质细胞活化和反应性神经胶质增生有助于限制脑损伤并重新建立中枢神经系统稳态。但是，神经胶质瘢痕形成会阻碍神经元的重新连接和延伸。神经炎症影响少突胶质细胞的脱髓鞘和再髓鞘。从少突胶质细胞释放的髓磷脂相关抗原激活外周T细胞，从而导致自身免疫反应。可以分化为少突胶质细胞的少突胶质前体细胞会发生缺血性中风，并可能导致功能恢复。在本文中，我们讨论了由神经胶质细胞介导的中风后免疫调节机制以及神经胶质细胞与神经元之间的相互作用。