Flow cytometric characterization of brain dendritic cell subsets after murine stroke

BACKGROUNDSterile inflammation is a substantial element of post-stroke pathophysiology with the determination of autoimmunity versus tolerance being one of its most important aspects. It is believed that this determination is initiated relatively early after stroke onset by clearing macrophages and...

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Published in:Experimental & translational stroke medicine Vol. 6; no. 1; p. 11
Main Authors: Pösel, Claudia, Uri, Anna, Schulz, Isabell, Boltze, Johannes, Weise, Gesa, Wagner, Daniel-Christoph
Format: Report
Language:English
Published: 01-01-2014
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Summary:BACKGROUNDSterile inflammation is a substantial element of post-stroke pathophysiology with the determination of autoimmunity versus tolerance being one of its most important aspects. It is believed that this determination is initiated relatively early after stroke onset by clearing macrophages and migratory dendritic cells (DC). However, the phenotypic differentiation of macrophages and DC is intricate particularly in the disease context. Here, we utilized a set of surface markers used in mucosal immunity research to investigate the involvement of macrophages and DC subpopulations in post-stroke inflammation in mice. FINDINGSPhotothrombotic stroke induced a significant increase of lineage (CD3, B220, Ly6G and CD49b) negative CD11b+ cells in the brain primarily consisting of F4/80+ macrophages and, to a lesser extent, F4/80-/CD11c-/CD11b+ monocytes and F4/80-/CD11c+ DC. The latter could be differentiated into the classical migratory DC subpopulations (CD11b+ and CD103+), but no CD4 or CD8+ DC were found. Finally, stroke caused a significant increase of CD11b/CD103 double-positive DC in the affected brain hemisphere. CONCLUSIONSThe surface marker combination used in this study allowed a phenotypic differentiation of macrophages and DC subpopulations after stroke, thus providing an important prerequisite to study post-stroke immunity and tolerance.
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ISSN:2040-7378
2040-7378
DOI:10.1186/2040-7378-6-11