Perinatal hypoxia-ischemia remains the primary cause of acute neonatal brain injury, leading to a high mortality rate and long-term neurological deficits, such as behavioral, social, attentional, cognitive and functional motor deficits. An ever-increasing body of evidence shows that the immune response to acute cerebral hypoxia-ischemia is a major contributor to the pathophysiology of neonatal brain injury. Hypoxia-ischemia provokes an intravascular inflammatory cascade that is further augmented by the activation of resident immune cells and the cerebral infiltration of peripheral immune cells response to cellular damages in the brain parenchyma. This prolonged and/or inappropriate neuroinflammation leads to secondary brain tissue injury. Yet, the long-term effects of immune activation, especially the adaptive immune response, on the hypoxic-ischemic brain still remain unclear. The focus of this review is to summarize recent advances in the understanding of post-hypoxic-ischemic neuroinflammation triggered by the innate and adaptive immune responses and to discuss how these mechanisms modulate the brain vulnerability to injury. A greater understanding of the reciprocal interactions between the hypoxic-ischemic brain and the immune system will open new avenues for potential immunomodulatory therapy in the treatment of neonatal brain injury.

围产期缺氧缺血仍然是新生儿急性脑损伤的主要原因，导致高死亡率和长期神经功能缺陷，如行为、社交、注意力、认知和功能运动缺陷。越来越多的证据表明，对急性脑缺氧缺血的免疫反应是新生儿脑损伤病理生理学的主要原因。缺氧缺血会引发血管内炎症级联反应，而常驻免疫细胞的激活和外周免疫细胞对脑实质细胞损伤的反应而进一步加剧炎症级联反应。这种长期和/或不适当的神经炎症会导致继发性脑组织损伤。然而，免疫激活，尤其是适应性免疫反应，对缺氧缺血大脑的长期影响仍不清楚。本综述的重点是总结对先天性和适应性免疫反应引发的缺氧缺血后神经炎症的理解的最新进展，并讨论这些机制如何调节大脑对损伤的脆弱性。更好地了解缺氧缺血性大脑与免疫系统之间的相互作用将为治疗新生儿脑损伤的潜在免疫调节疗法开辟新途径。