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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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All trans-retinoic acid protects against acute ischemic stroke by modulating neutrophil functions through STAT1 signaling

TL;DR: atRA displays potent therapeutic efficacy in ischemic stroke by attenuating neural inflammation and downregulated neutrophil accumulation and STAT1 signaling played a decisive role in the mechanisms of atRA-afforded regulation to neutrophils.
Journal ArticleDOI

Experimental ischemic stroke induces long-term T cell activation in the brain.

TL;DR: The results indicated a prolonged activation of brain invading CD4+ and CD8+ T cells after ischemic stroke which may play a role in the neural repair process after stroke.
Journal ArticleDOI

Prokineticin 2 is an endangering mediator of cerebral ischemic injury

TL;DR: It is indicated that prokineticin 2 can be activated by pathological stimuli such as hypoxia-ischemia and excitotoxic glutamate and identified PK2 as a deleterious mediator for cerebral ischemia.
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Emerging Role of Immunity in Cerebral Small Vessel Disease.

TL;DR: The findings suggest that antigen-specific immune responses could occur in CSVD, and that autoimmune activity should be assessed in future studies; this knowledge would benefit the development of effective therapeutic interventions inCSVD.
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Tissue-Resident Ecto-5′ Nucleotidase (CD73) Regulates Leukocyte Trafficking in the Ischemic Brain

TL;DR: To define the CD73-bearing cells responsible for ischemic cerebroprotection, mice were subjected to irradiative myeloablation, marrow reconstitution, and then stroke following engraftment to show a cardinal role for CD73 in suppressing isChemic tissue leukosequestration.
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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