Key result
Permanent stroke triggers delayed T-cell and macrophage infiltration into the infarct core and corpus callosum.
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Reveals delayed peak infiltration of T-cells and macrophages weeks after experimental stroke in mice, suggesting prolonged adaptive immune responses during post-stroke recovery.
The activities of the central and peripheral immune systems impact neurological outcome after ischemic stroke. However, studies investigating the temporal profile of leukocyte infiltration, especially T‐cell recruitment, are sparse. Our aim was to investigate leukocyte infiltration at different time points after experimental stroke in mice. Permanent middle cerebral artery occlusion was performed on 11 weeks old C57BL/6J mice, allowed to survive for 1, 3, 8, 14 or 28 days. In addition to infarct size measurements, detailed immunohistochemical analyses of T‐cell and macrophage influx were performed. A recently introduced F‐19 MR probe (V‐sense), designed to track macrophages, was furthermore tested. Fourteen and 28 days after permanent middle cerebral artery occlusion a significant increase in CD3 + T‐cells was found within the ipsilateral hemisphere compared to controls, especially within the infarct core and the corpus callosum. The number of CD68 + cells within the infarct core was significantly increased at days 8, 14 and 28. This temporal pattern was also seen in MRI. After experimental stroke within the infarcted cortex we found a delayed (day 14) infiltration of T‐cells and macrophages. Furthermore, our data show that T‐cells are present in higher numbers in the corpus callosum compared to the rest of the brain (except from the infarct core where they were highest).
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Sørensen et al. (2017) studied Experimental ischemic stroke (permanent middle cerebral artery occlusion in mice). Permanent middle cerebral artery occlusion (experimental stroke) and F-19 MR probe (V-sense) vs. Controls was evaluated on Temporal and spatial infiltration of CD3+ T-cells and CD68+ macrophages. Permanent middle cerebral artery occlusion in mice induced delayed infiltration of CD3+ T-cells (days 14 and 28) and CD68+ macrophages (days 8, 14, and 28) in the infarct core and corpus callosum.
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