Table 1.
Effects of immune cells in immune responses after cerebral ischemia.
| Immune cell | Effects in cerebral post-ischemic responses | |
|---|---|---|
| Neutrophils | (1) Promote immune cell recruitment to the ischemic region, including lymphocytes, monocytes, and platelets; (2) Clearance of dead cells, debris, and bacteria as a defense against the increased risk of infection as a result of immunosuppression after stroke; (3) Involved in tissue repair and remodeling processes | |
| T lymphocytes | (1) Infiltrate into infarct areas to promote ischemic injury via IL-17, IL-23, and IL-33 secreted by γδT cells; (2) Produce IL-2 to reduce Th17 production by CD4+ T cells | |
| Regulatory T cells | (1) Reduce immune cell infiltration; (2) Promote neovascularization; (3) Promote immunosuppression | |
| B lymphocytes | (1) Inhibit the activation and recruitment of other immune cells; (2) Promote the recovery process; (3) Harmful to long-term recovery and probably lead to delayed neurological and cognitive function deficits. | |
| Regulatory B cells | (1) Down-regulate macrophage cytokine production; (2) Suppress pro-inflammatory T cells and enhance the expansion of regulatory T cells; (3) Promote Th2 polarization via IL-12 | |
| NK cells | (1) Participate in Th1 priming of CD4+ T cells; (2) Kill recently activated CD8+ T cells in an NKG2D- and perforin-dependent manner; (3) Promote neuronal death | |
| Astrocytes | (1) Produce IL-15, mediating Th1 polarization of CD4+ T cells, enhancing production of Tregs, and influencing maturation of NK cells; (2) Activation aggravates ischemic injury | |
| Macrophages /microglia |
Residental microglia | (1) Prompt microglial M1 polarization and neutrophil recruitment; (2) Induce neuron death through TNF-α; (3) Migrate from infarct center to peri-infarct regions in delayed phase |
| Infiltrated macrophages | (1) CD14+ differentiation induces CD4+ T cell polarization into Th-17 cells when migrating across the BBB via TGF-β and GM-CSF; (2) Display anti-inflammatory, phagocytic and wound healing function in early phase; (3) Migrate from infarct center and tend to display an M2-like phenotype in delayed phases | |