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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

Peripheral immune cells infiltrate into sites of secondary neurodegeneration after ischemic stroke.

TL;DR: Investigating whether immune cells are present in sites of SND and, if so, how these cell populations compare to those in the peri-infarct zone indicates that infiltrating immune cells persist in ischemic tissue after the acute isChemic phase, and are increased in sitesof SND.
Journal ArticleDOI

Brain-gut axis after stroke.

TL;DR: Recent advances in the studies of the brain–gut axis after stroke are discussed, the key issues to be solved, and the future directions.
Journal ArticleDOI

Role of Immune Cells Migrating to the Ischemic Brain

TL;DR: This review will focus on neutrophils, monocyte/macrophages, and T and NK (natural killer) lymphocytes, which are the innate immune cells resident in the brain parenchyma and are regarded as targets for therapeutic intervention in acute stroke.
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Carcinoembryonic Antigen–Related Cell Adhesion Molecule 1 Inhibits MMP-9–Mediated Blood–Brain–Barrier Breakdown in a Mouse Model for Ischemic Stroke

TL;DR: CEACAM1 is proposed as an important inhibitory regulator of neutrophil-mediated tissue damage and BBB breakdown in focal cerebral ischemia and neutralization of matrix metalloproteinase-9 activity in Ceacam1−/− mice was sufficient to alleviate stroke sizes and improve survival to the level of CEACam1-competent animals.
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De novo expression of dopamine D2 receptors on microglia after stroke

TL;DR: It is found that cultured primary microglia express dopamine D1, D2, D3, D4, and D5 receptors, and the D2/3R agonist, pramipexole, enhanced the secretion of nitrite by culturedmicroglia in response to proinflammatory stimuli, suggesting that dopamine may serve as a modulator of microglial function during neuroinflammation.
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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