Figure 1.

Schematic diagram of mechanisms of stroke-induced immunosuppression with NK cells as an example. In the early stages of stroke (<24 hours), ischaemic neuron-recruited NK cells are swiftly mobilised into ischaemic areas, where they promote neuronal death (not shown in figure).³⁴ Subsequently (>48 hours?), ischaemic neuron-derived signals can turn off NK cells that express neurotransmitter receptors. At the peripheral level, ischaemic brain injury influences the sympathetic, parasympathetic (vagus nerve) and/or hypothalamic-pituitary-adrenal (HPA) axis systems that suppress NK cell-mediated immunity. Differences in the spectrum of neurogenic innervations, immune cell subsets and soluble mediators in the CNS versus the periphery may differentially affect _NK cell deficiency in these two compartments. BBB, blood brain barrier; BDNF, brain-derived neurotrophic factor; CNS, central nervous system; EGF, epithelial growth factor; GABA, gamma-aminobutyric acid; NK, natural killer; UTP, uridine triphosphate.