The Involvement and Therapy Target of Immune Cells After Ischemic Stroke

Jian, Zhihong; Liu, Rui; Zhu, Xinqun; Smerin, Daniel; Zhong, Yi; Gu, Lijuan; Fang, Weirong; Xiong, Xiaoxing

doi:10.3389/fimmu.2019.02167

Cited by 177 publications

(195 citation statements)

References 149 publications

(181 reference statements)

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“…The main sources of macrophages infiltrating into ischaemic brain tissue after stroke include microglia-derived macrophages (MiDM) and monocyte-derived macrophages (MoDM). Peripheral monocytes are migrated through the BBB to the ischaemic brain under the action of chemokines and cell adhesion molecules [87].…”

Section: Microglial Responses In Ischaemic Strokementioning

confidence: 99%

“…Microglia that exhibit anti-oxidative responses, including suppressing the post-ischaemic level of ROS, and upregulating GSH and heme oxygenase-1 (HO-1), which inhibit oxidation of phosphatidylserine (PS), promote viable neuron repair [70]. In contrast, microglia that possess high levels of ROS have an increased capacity to phagocytose potentially viable neuron [85,87].…”

Section: Microglial Responses In Ischaemic Strokementioning

confidence: 99%

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Post-Ischaemic Immunological Response in the Brain: Targeting Microglia in Ischaemic Stroke Therapy

et al. 2020

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Microglia, the major endogenous immune cells of the central nervous system, mediate critical degenerative and regenerative responses in ischaemic stroke. Microglia become “activated”, proliferating, and undergoing changes in morphology, gene and protein expression over days and weeks post-ischaemia, with deleterious and beneficial effects. Pro-inflammatory microglia (commonly referred to as M1) exacerbate secondary neuronal injury through the release of reactive oxygen species, cytokines and proteases. In contrast, microglia may facilitate neuronal recovery via tissue and vascular remodelling, through the secretion of anti-inflammatory cytokines and growth factors (a profile often termed M2). This M1/M2 nomenclature does not fully account for the microglial heterogeneity in the ischaemic brain, with some simultaneous expression of both M1 and M2 markers at the single-cell level. Understanding and regulating microglial activation status, reducing detrimental and promoting repair behaviours, present the potential for therapeutic intervention, and open a longer window of opportunity than offered by acute neuroprotective strategies. Pharmacological modulation of microglial activation status to promote anti-inflammatory gene expression can increase neurogenesis and improve functional recovery post-stroke, based on promising preclinical data. Cell-based therapies, using preconditioned microglia, are of interest as a method of therapeutic modulation of the post-ischaemic inflammatory response. Currently, there are no clinically-approved pharmacological options targeting post-ischaemic inflammation. A major developmental challenge for clinical translation will be the selective suppression of the deleterious effects of microglial activity after stroke whilst retaining (or enhancing) the neurovascular repair and remodelling responses of microglia.

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Section: Microglial Responses In Ischaemic Strokementioning

confidence: 99%

Section: Microglial Responses In Ischaemic Strokementioning

confidence: 99%

Post-Ischaemic Immunological Response in the Brain: Targeting Microglia in Ischaemic Stroke Therapy

et al. 2020

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“…One of the important factors for both of these effects is time. Jian et al, stated that in the early stage after the stroke, microglia are recruited, while peripheral immune cells appear within one day (neutrophils even within the first hour) and lasting until seven days after the stroke event [ 6 ]. The CD8 + T cells appear 3 h after the stroke at earliest, while CD4 + T cells within 24 h after the stroke.…”

Section: Inflammation and Immunomodulation As Treatment Modes In Smentioning

confidence: 99%

Genetic Aspects of Inflammation and Immune Response in Stroke

Nikolić

Janković

Petrović³

et al. 2020

IJMS

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Genetic determinants play important role in the complex processes of inflammation and immune response in stroke and could be studied in different ways. Inflammation and immunomodulation are associated with repair processes in ischemic stroke, and together with the concept of preconditioning are promising modes of stroke treatment. One of the important aspects to be considered in the recovery of patients after the stroke is a genetic predisposition, which has been studied extensively. Polymorphisms in a number of candidate genes, such as IL-6, BDNF, COX2, CYPC19, and GPIIIa could be associated with stroke outcome and recovery. Recent GWAS studies pointed to the variant in genesPATJ and LOC as new genetic markers of long term outcome. Epigenetic regulation of immune response in stroke is also important, with mechanisms of histone modifications, DNA methylation, and activity of non-coding RNAs. These complex processes are changing from acute phase over the repair to establishing homeostasis or to provoke exaggerated reaction and death. Pharmacogenetics and pharmacogenomics of stroke cures might also be evaluated in the context of immuno-inflammation and brain plasticity. Potential novel genetic treatment modalities are challenged but still in the early phase of the investigation.

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“…Microglia and blood-borne macrophages play major roles in the pathophysiological processes in various kinds of pathologies of the central nervous system (CNS) by releasing numerous bioactive substances, including cytokines, growth factors, and reactive oxygen/nitrogen species, and phagocytosing degenerating cells and materials [1][2][3][4] . In this article, we use "microglia" to denote resident microglia in the CNS, and "macrophages" to denote cells derived from circulating monocytes that have invaded (typically inflamed) CNS lesions with a disrupted blood-brain barrier (BBB).…”

Section: Introductionmentioning

confidence: 99%

“…In this review, "favorable" is used to describe microglia and macrophages that are neuroprotective cells bringing about the better outcome in the pathologic CNS than "unfavorable" ones that exert deleterious effects on the survival of neurons and other parenchymal cells. Therefore, various kinds of interventions, including pharmacological treatment and rehabilitation, have been studied in laboratory and clinical settings to determine if they enhance favorable responses while also suppressing the deleterious effects of microglia and macrophages [1,4,13,14] . This aim may be interpreted as attempting to induce M2-polarized or alternatively activated phenotypes of these cells [15][16][17] .…”

Section: Introductionmentioning

confidence: 99%

Favorable and unfavorable roles of microglia and macrophages in the pathologic central nervous system

Tanaka¹

2020

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How to cite this article: Tanaka J. Favorable and unfavorable roles of microglia and macrophages in the pathologic central nervous system. Neuroimmunol Neuroinflammation 2020;7:73-91. http://dx. AbstractResident microglia in the central nervous system (CNS) are activated rapidly in response to even minor pathologic changes in the CNS, releasing various cytokines, growth factors, reactive oxygen species and other bioactive substances, in addition to eliminating synapses and degenerating cells through phagocytosis. Monocytes in circulation invade the inflamed brain tissues and develop into macrophages that also produce several bioactive substances and engage in phagocytosis. This article introduces methods for distinguishing microglia and macrophages. The pathophysiological roles of resident microglia and macrophages are discussed in animal models with neuroinflammation in the brain either with or without disruption of the blood-brain barrier. Both cell types have ameliorating and aggravating effects on the pathologic CNS, and their different roles are addressed in this article. Furthermore, this article compares the effects of some pharmacological interventions to induce phenotypic cellular changes for improved outcomes of the pathologic CNS.

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The Involvement and Therapy Target of Immune Cells After Ischemic Stroke

Cited by 177 publications

References 149 publications

Post-Ischaemic Immunological Response in the Brain: Targeting Microglia in Ischaemic Stroke Therapy

Post-Ischaemic Immunological Response in the Brain: Targeting Microglia in Ischaemic Stroke Therapy

Genetic Aspects of Inflammation and Immune Response in Stroke

Favorable and unfavorable roles of microglia and macrophages in the pathologic central nervous system

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