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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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Journal ArticleDOI

Spectratype analysis of clonal T cell expansion in murine experimental stroke.

TL;DR: This is the first study presenting direct evidence of clonal T cell expansion after stroke - however, with delayed kinetics that make antigen-dependent mechanisms unlikely in acute post-ischemic neuroinflammation.
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Deficiency in serine protease inhibitor neuroserpin exacerbates ischemic brain injury by increased postischemic inflammation.

TL;DR: Excessive microglial activation in Ns−/− mice mediated by an increased activity of tPA results in a worse outcome further underscoring the potential detrimental proinflammatory effects of t PA.
Journal ArticleDOI

Immune changes in peripheral blood and hematoma of patients with intracerebral hemorrhage

TL;DR: Results indicate that immunocytes present in the hematoma may participate in the acute‐phase inflammatory response after ICH, and increased levels of IL‐10 in the serum and Hematoma, and a reduction in M1‐like macrophages in hematomas were independently associated with favorable outcome on day 90.
Journal ArticleDOI

The Paradox Role of Regulatory T Cells in Ischemic Stroke

TL;DR: Tregs contributed to the outcome of ischemic stroke, while more lines of evidence are needed to understand how Tregs regulate the immune system and influence the outcomes of stroke.
Journal ArticleDOI

Mechanism underlying treatment of ischemic stroke using acupuncture: transmission and regulation.

TL;DR: The overall conditions of inflammatory cells, mediators, and pathways after cerebral ischemia/reperfusion are summarized, and the possible synergistic intervention of acupuncture in the inflammatory signaling pathway network is discussed to provide a foundation to explore the multiple molecular mechanisms by which acupuncture promotes nerve function restoration.
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.
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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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