Immune response in cerebral ischemic injury: interaction and therapeutic potential

Cerebral ischemia primarily results from vascular stenosis or blockage, which activates inflammatory cells and triggers an immune response. An excessive immune response can exacerbate the damage caused by cerebral ischemia. In this review, the keywords “immune response” and “cerebral ischemia” were entered into the PubMed database, yielding 241 articles, of which 141 were included in the analysis. Relevant literature from 2021 to 2024 was summarized, classified, and synthesized to delineate advancements in this field. Consequently, in exploring the basic physiology of immune responses and brain injury, we found that microglia can phagocytose dead neurons, thereby ameliorating ischemic brain injury. However, inflammatory cells accumulate and attack blood vessels and nerve cells following cerebral ischemia, resulting in additional damage. As a result, targeting CD8 T cells, astrocytes, superoxide dismutase (SOD), interleukin-10 (IL-10), tumor necrosis factor (TNF), NLRP3, and the NF-κB signaling pathway can help mitigate this damage. Furthermore, the specific mechanisms and efficacy of therapeutic drugs in recent years were analyzed, revealing their potential to repair the blood-brain barrier, endothelial cells, and neurons, while also reducing infarct size and inflammatory responses. Together, we highlight that immune cells, particularly microglia, present new therapeutic breakthroughs in neuron phagocytosis, improvement of inflammatory responses, and reduction of vascular endothelial damage. These findings provide clinicians and researchers with cutting-edge references for treatment strategies.