ArticleStroke2026
Immune Checkpoint B7-H3 Inhibition Reprograms Acute Neuroinflammation and Protects the Brain After Acute Ischemic Stroke.
Article in Stroke, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundThe role of immune checkpoint B7-H3 in acute ischemic stroke prognosis and poststroke immunosuppression remains uninvestigated, despite the clinical significance of immune checkpoints with inflammaging and poststroke infections. In this study, we investigated the effect of regulating cerebral induction of B7-H3 after acute ischemic stroke and evaluated its longitudinal impact on brain damage, neuroinflammation, vascular integrity, host defense gene regulation, and functional outcomes.
methodsC57BL/6 mice were subjected to transient middle cerebral artery occlusion and injected (intravenously) with either B7-H3 small interfering RNA or a negative (nontargeting) small interfering RNA at 5 minutes after reperfusion. On poststroke days 1, 3, and 7, magnetic resonance imaging of the mouse brain was performed using a 9.4-T scanner to assess brain damage (T2, apparent diffusion coefficient, and kurtosis) and blood-brain barrier integrity (T1 with contrast). Real-time quantitative polymerase chain reaction and NanoString nCounter neuroinflammation panels were used to determine acute changes in overall neuroinflammatory functions mediated by B7-H3. Motor function was assessed between days 1 and 7 of reperfusion.
resultsEarly inhibition of B7-H3 after stroke significantly reduced blood-brain barrier disruption and brain damage and promoted functional outcomes. Poststroke neuroinflammation was reprogrammed with B7-H3 inhibition to balance neuroprotective anti-inflammatory mechanisms without compromising the immune response, which is crucial for preventing poststroke infections.
conclusionsThe longitudinal assessment of blood-brain barrier, infarction, and proinflammatory cytokines demonstrates that B7-H3 induction during the acute period after stroke mediates poststroke neuroinflammation and secondary brain damage.
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