Reciprocal interactions between peripheral and central immune cells across different stages of ischemic stroke: mechanisms, influencing factors and research progress

Ischemic stroke (IS), characterised by vascular occlusion, is the most common type of stroke. Focal cerebral ischemia triggers a robust immune response, with immune cells and the associated inflammatory reactions emerging shortly after the ischemic event and persisting over time. The inflammatory mediators released during this process not only induce immune dysregulation but also exacerbate brain injury, adversely affecting post-stroke prognosis. Although increasing attention has been directed toward the interactions between the central nervous system and peripheral immunity following stroke, the progression of inflammation and the intercellular interactions among immune cells during the acute and chronic phases of ischemia remain insufficiently understood. Therefore, this review takes peripheral immune cells (T lymphocytes, neutrophils, B cells, and natural killer cells) as examples to summarise the dynamic interrelationships and influences between peripheral immune cells and central immune cells (microglia and astrocytes) at different stages following IS. The mechanisms underlying these immune cell interactions and the cytokines involved are discussed, with illustrative examples. Additionally, the impact of comorbidities on the progression of IS is explored, providing insights for further research on the interplay between the central nervous system and peripheral immunity.