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Front Aging Neurosci. 2016 Feb 22;8:29. doi: 10.3389/fnagi.2016.00029. eCollection 2016.

The Role of Monocytes in Ischemic Stroke Pathobiology: New Avenues to Explore.

Author information

1
Neuroscience Axis, CHU de Québec Research Center (CHUL)Québec City, QC, Canada; Department of Psychiatry and Neuroscience, Faculty of Medicine, Laval UniversityQuébec City, QC, Canada.
2
Department of Psychiatry and Neuroscience, Faculty of Medicine, Laval University Québec City, QC, Canada.

Abstract

Ischemic stroke accounts for the majority of stroke cases and constitutes a major cause of death and disability in the industrialized world. Inflammation has been reported to constitute a major component of ischemic stroke pathobiology. In the acute phase of ischemic stroke, microglia, the resident macrophages of the brain, are activated, followed by several infiltration waves of different circulating immune cells into the brain. Among these circulating immune cells, monocytes have been shown to play a particularly important role. Following their infiltration, monocytes differentiate into potent phagocytic cells, the monocyte-derived macrophages (MDMs), in the ischemic brain. Initially, the presence of these cells was considered as marker of an exacerbated inflammatory response that contributes to brain damage. However, the recent reports are suggesting a more complex and multiphasic roles of these cells in ischemic stroke pathobiology. Monocytes constitute a heterogeneous group of cells, which comprises two major subsets in rodent and three major subsets in human. In both species, two equivalent subsets exist, the pro-inflammatory subset and the anti-inflammatory subset. Recent data have demonstrated that ischemic stroke differentially regulate monocyte subsets, which directly affect ischemic stroke pathobiology and may have direct implications in ischemic stroke therapies. Here, we review the recent findings that addressed the role of different monocyte subsets in ischemic stroke pathobiology, and the implications on therapies.

KEYWORDS:

inflammation; ischemic stroke; monocytes; neuronal damage; neurorestoration

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