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. 2017 Aug 2;6(8):e006387. doi: 10.1161/JAHA.117.006387

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© 2017 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.

This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

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Schematic overview of the proposed mechanism of CCR5‐mediated Treg docking and activation at the ischemic blood‐brain barrier. In response to cerebral ischemic stroke, the endothelial cells express CCL5, which mediates the adoptively transferred Tregs to dock at the ischemic blood‐brain barrier. Once engaged with CCL5, CCR5 is activated and upregulates the expression of PD‐L1 on Tregs, which inhibits the production of MMP‐9 from neutrophils. As a result, CCR5 signaling contributes to Treg‐afforded protection of the blood‐brain barrier after ischemic stroke. CCL5 indicates ligand for CCR5; CCR5, C‐C chemokine receptor type 5; Treg, regulatory T cell.