Cerebral ischemia may cause irreversible neural network damage and result in functional deficits. Targeting neuronal repair after stroke potentiates the formation of new connections, which can be translated into a better functional outcome. Innate and adaptive immune responses in the brain and the periphery triggered by ischemic damage participate in regulating neural repair after a stroke. Immune cells in the blood circulation and gut lymphatic tissues that have been shaped by immune components including gut microbiota and metabolites can infiltrate the ischemic brain and, once there, influence neuronal regeneration either directly or by modulating the properties of brain-resident immune cells. Immune-related signalings and metabolites from the gut microbiota can also directly alter the phenotypes of resident immune cells to promote neuronal regeneration. In this review, we discuss several potential mechanisms through which peripheral and brain-resident immune components can cooperate to promote first the resolution of neuroinflammation and subsequently to improved neural regeneration and a better functional recovery. We propose that new insights into discovery of regulators targeting pro-regenerative process in this complex neuro-immune network may lead to novel strategies for neuronal regeneration.

脑缺血可能引起不可逆的神经网络损害并导致功能缺陷。中风后靶向神经元修复可增强新连接的形成，这可以转化为更好的功能结局。缺血性损伤触发的大脑和周围区域的先天性和适应性免疫反应参与中风后神经修复的调节。免疫系统（包括肠道菌群和代谢产物）形成的血液循环和肠道淋巴组织中的免疫细胞可以浸润缺血性大脑，并且一旦进入那里，就会直接或通过调节驻留于大脑的免疫细胞的性质影响神经元的再生。来自肠道菌群的免疫相关信号和代谢产物也可以直接改变驻留免疫细胞的表型，从而促进神经元再生。在这篇综述中，我们讨论了几种潜在的机制，外周和大脑驻留的免疫成分可以通过这些机制进行协作，以首先促进神经炎症的解决，进而促进神经再生和更好的功能恢复。我们提出，在这种复杂的神经免疫网络中，针对调节促再生过程的调节剂的发现有新见解，可能会导致神经元再生的新策略。我们讨论了几种潜在的机制，外周和大脑驻留的免疫成分可以通过这些机制进行协作，以首先促进神经炎症的解决，然后促进神经再生和更好的功能恢复。我们提出，在这种复杂的神经免疫网络中，针对调节促再生过程的调节剂的发现有新见解，可能会导致神经元再生的新策略。我们讨论了几种潜在的机制，外周和大脑驻留的免疫成分可以通过这些机制进行协作，以首先促进神经炎症的解决，然后促进神经再生和更好的功能恢复。我们建议对这种复杂的神经免疫网络中针对促再生过程的调节子的发现进行新的探索，可能会导致神经元再生的新策略。