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Temporal and Spatial Dynamics of Cerebral Immune Cell Accumulation in Stroke

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TLDR
The peculiar activation pattern and massive increase of antigen-presenting cells in temporal conjunction with regulatory cells might provide additional insight into poststroke immune regulation.
Abstract
Background and Purpose— Ischemic stroke leads to significant morbidity and mortality in the Western world Early reperfusion strategies remain the treatment of choice but can initiate and augment an inflammatory response causing secondary brain damage The understanding of postischemic inflammation is very limited The objectives of this study were to define the temporal and spatial infiltration of immune cell populations and their activation patterns in a murine cerebral ischemia–reperfusion injury model Methods— Transient middle cerebral artery occlusion was induced for 1 hour followed by 12-hour to 7-day reperfusion in C57/BL6 mice Immunohistochemistry and flow cytometry were used to quantify the infiltrating immune cell subsets Results— Accumulation of microglia and infiltration of the ischemic hemisphere by macrophages, lymphocytes, and dendritic cells (DCs) preceded the neutrophilic influx DCs were found to increase 20-fold and constituted a substantial proportion of infiltrating cells DCs exhi

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Citations
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Crosstalk between microglia and T cells contributes to brain damage and recovery after ischemic stroke

TL;DR: Extensive evidence supports a critical role for the crosstalk of microglia and T cells in the prognosis of brain injury after ischemic stroke, and the regulation of the c Crosstalk may provide a potential therapeutic target for improving the isChemic brain damage.
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P2Y6 receptor inhibition aggravates ischemic brain injury by reducing microglial phagocytosis

TL;DR: Clearance of damaged cells and debris is beneficial for the functional recovery after ischemic brain injury, however, the specific phagocytic receptor that mediates microglialphagocytosis after isChemic stroke is unknown.
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Evolution of ischemic damage and behavioural deficit over 6 months after MCAo in the rat: Selecting the optimal outcomes and statistical power for multi-centre preclinical trials.

TL;DR: This study investigates the development of ischemic damage after thread occlusion MCAo in the rat, using histological and behavioural outcomes and the adhesive removal test to investigate the longevity of behavioural deficit after isChemic stroke in rats, and examines the practicality of using such measures as the primary outcome for future studies.
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Classification of Microglial Morphological Phenotypes Using Machine Learning.

TL;DR: In this paper, a novel microglial classification method by morphological evaluation using a convolutional neuronal network on the basis of manually selected cells in addition to classical morphological parameters was described.
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CCR6 (CC Chemokine Receptor 6) Is Essential for the Migration of Detrimental Natural Interleukin-17-Producing γδ T Cells in Stroke.

TL;DR: It is demonstrated that therapeutic approaches targeting synergistic IL-17 and tumor necrosis factor-&agr; pathways in parallel offer additional neuroprotection in stroke, and brain-infiltrating IL-18–positive T cells belong to the subset of natural IL- 17–producing T cells.
References
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Journal ArticleDOI

Pathobiology of ischaemic stroke: an integrated view

TL;DR: This article provides a framework that can be used to generate testable hypotheses and treatment strategies that are linked to the appearance of specific pathophysiological events within the ischaemic brain.
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Microglia: active sensor and versatile effector cells in the normal and pathologic brain

TL;DR: This review focuses on several key observations that illustrate the multi-faceted activities of microglia in the normal and pathologic brain.
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Taking dendritic cells into medicine

TL;DR: Some medical implications of DC biology that account for illness and provide opportunities for prevention and therapy are presented.
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The inflammatory response in stroke.

TL;DR: The role of specific cell types including leukocytes, endothelium, glia, microglia, the extracellular matrix and neurons, and mediators produced by inflammatory cells such as cytokines, chemokines, reactive oxygen species and arachidonic acid metabolites are reviewed.
Journal ArticleDOI

A synthetic glycolipid prevents autoimmune encephalomyelitis by inducing TH2 bias of natural killer T cells.

TL;DR: A synthetic glycolipid ligand for CD1d-restricted natural killer T (NKT) cells expressing the semi-invariant T-cell receptor (Vα14+) is preventive against EAE and targeting NKT cells with this ligand may be an attractive means for intervening in human autoimmune diseases such as multiple sclerosis.
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