NK cells in cerebral ischemia

Chen, Chen; Ai, Qidi; Chu, Shifeng; Zhang, Zhao; Chen, Nai‐Hong

doi:10.1016/j.biopha.2018.10.103

Cited by 42 publications

(38 citation statements)

References 90 publications

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“…Analysis of Cx3cr 1 GFP/+ Ccr2 RFP/+ mice allows for simultaneous tracking of green fluorescent protein (GFP + ) microglia and red fluorescent protein (RFP + ) peripheral monocytes/macrophages (Mo/MΦ) and polymorphonuclear neutrophils (PMNs) that have trafficked to ischemic brain 32 . CD11b + myeloid cells were stained with anti-CD45, to distinguish CD45 int -resident microglia from CD45 hi peripherally derived Mo/MΦ, anti-Ly6G, to identify PMNs, and were evaluated for GFP and RFP expression; NK cells, which are CD11b + non-myeloid cells and infiltrate the ischemic hemisphere 33 , were not evaluated in this study (Fig. 1c).…”

Section: Resultsmentioning

confidence: 99%

Peripheral TREM1 responses to brain and intestinal immunogens amplify stroke severity

et al. 2019

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Stroke is a multiphasic process in which initial cerebral ischemia is followed by secondary injury from immune responses to ischemic brain components. Here we demonstrate that peripheral CD11b + CD45 + myeloid cells magnify stroke injury via activation of triggering receptor expressed on myeloid cells 1 (TREM1), an amplifier of proinflammatory innate immune responses. TREM1 was induced within hours after stroke peripherally in CD11b + CD45 + cells trafficking to ischemic brain. TREM1 inhibition genetically or pharmacologically improved outcome via protective antioxidant and anti-inflammatory mechanisms. Positron electron tomography imaging using radiolabeled antibody recognizing TREM1 revealed elevated TREM1 expression in spleen and, unexpectedly, in intestine. In the lamina propria, noradrenergic-dependent increases in gut Reprints and permissions information is available at www.nature.com/reprints.

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Section: Resultsmentioning

confidence: 99%

Peripheral TREM1 responses to brain and intestinal immunogens amplify stroke severity

et al. 2019

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“…Peripheral infiltrating immune cells are pivotal in the inflammatory responses in primary infarct area after stroke (95)(96)(97)(98). At present, only one study reports the involvement of peripheral infiltrating immune cells in the secondary thalamic injury.…”

Section: Peripheral Immune Cellsmentioning

confidence: 99%

Inflammatory Responses in the Secondary Thalamic Injury After Cortical Ischemic Stroke

et al. 2020

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Stroke is one of the major causes of chronic disability worldwide and increasing efforts have focused on studying brain repair and recovery after stroke. Following stroke, the primary injury site can disrupt functional connections in nearby and remotely connected brain regions, resulting in the development of secondary injuries that may impede long-term functional recovery. In particular, secondary degenerative injury occurs in the connected ipsilesional thalamus following a cortical stroke. Although secondary thalamic injury was first described decades ago, the underlying mechanisms still remain unclear. We performed a systematic literature review using the NCBI PubMed database for studies that focused on the secondary thalamic degeneration after cortical ischemic stroke. In this review, we discussed emerging studies that characterized the pathological changes in the secondary degenerative thalamus after stroke; these included excitotoxicity, apoptosis, amyloid beta protein accumulation, blood-brain-barrier breakdown, and inflammatory responses. In particular, we highlighted key findings of the dynamic inflammatory responses in the secondary thalamic injury and discussed the involvement of several cell types in this process. We also discussed studies that investigated the effects of blocking secondary thalamic injury on inflammatory responses and stroke outcome. Targeting secondary injuries after stroke may alleviate network-wide deficits, and ultimately promote stroke recovery.

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“…2 c). This finding is particularly clinically relevant as depletion of systemic NK cells early after stroke due to their mobilization to the ischemic brain and their local inflammatory activity has been associated with post-stroke recovery 30 , 31 .…”

Section: Resultsmentioning

confidence: 99%

VoPo leverages cellular heterogeneity for predictive modeling of single-cell data

et al. 2020

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High-throughput single-cell analysis technologies produce an abundance of data that is critical for profiling the heterogeneity of cellular systems. We introduce VoPo (https://github. com/stanleyn/VoPo), a machine learning algorithm for predictive modeling and comprehensive visualization of the heterogeneity captured in large single-cell datasets. In three mass cytometry datasets, with the largest measuring hundreds of millions of cells over hundreds of samples, VoPo defines phenotypically and functionally homogeneous cell populations. VoPo further outperforms state-of-the-art machine learning algorithms in classification tasks, and identified immune-correlates of clinically-relevant parameters.

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NK cells in cerebral ischemia

Cited by 42 publications

References 90 publications

Peripheral TREM1 responses to brain and intestinal immunogens amplify stroke severity

Peripheral TREM1 responses to brain and intestinal immunogens amplify stroke severity

Inflammatory Responses in the Secondary Thalamic Injury After Cortical Ischemic Stroke

VoPo leverages cellular heterogeneity for predictive modeling of single-cell data

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