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. 2018 Dec 11;243(17-18):1302–1312. doi: 10.1177/1535370218818172

Table 1.

Potential therapies to target glial–immune interactions post-ischemic stroke.

Therapy Known use Target/action Overall effect
Minocycline82–87 Bacteriostatic antibiotic MicrogliaSelectively inhibits M1 phenotype Anti-inflammatory Neuroprotective
PD-L1:PD-1 pathway9 Not currently used as a therapy Inhibits CD8+ T-cell activation and cytokine production Neuroprotective
Anti-CD8+Anti-NK1.1 antibodiesAnti-IL-15 antibodies4,68 Not currently used as a therapy Blocks interaction of astrocyte transpresentation of IL-15 to T-cells and NK cells Decrease infarct volume
L-histidine/histamine10,45–47,54–57,59,60 Likely has significant side effects; not in use Microglia and astrocytesPrevent disruption of Oct3Increase migration of regulatory T-cells to ischemic regions Decrease infarct volumeNeuroprotectiveAnti-inflammatory

IL-15: interleukin 15; PD-L1: programmed death-ligand 1; PD-1: programmed death-1; NK: natural killer; CD: cluster of differentiation; Oct3: organic cation transporter 3.