The roles of macrophages and microglia in multiple sclerosis and experimental autoimmune encephalomyelitis

Chu, Fengna; Shi, Mingchao; Chen, Zheng; Shen, Donghui; Zhu, Jie; Zheng, Xiangyu; Cui, Li

doi:10.1016/j.jneuroim.2018.02.015

Cited by 259 publications

(170 citation statements)

References 89 publications

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“…As the resident macrophages of the central nervous system (CNS), microglia play a vital role in regulating inflammation, balancing immunity, and promoting development and tissue repair. It is believed that an M1/M2 phenotype imbalance occurs in the CNS diseases and that the polarization of microglia from the M1 to M2 phenotypes can maintain immune homeostasis and neurological function in patients with CNS diseases (103).…”

Section: Microgliamentioning

confidence: 99%

Immunoregulatory Effects of Stem Cell-Derived Extracellular Vesicles on Immune Cells

Xie

Wang²,

She

et al. 2020

Front. Immunol.

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Recent investigations on the regulatory action of extracellular vesicles (EVs) on immune cells in vitro and in vivo have sparked interest on the subject. As commonly known, EVs are subcellular components secreted by a paracellular mechanism and are essentially a group of nanoparticles containing exosomes, microvesicles, and apoptotic bodies. They are double-layer membrane-bound vesicles enriched with proteins, nucleic acids, and other active compounds. EVs are recognized as a novel apparatus for intercellular communication that acts through delivery of signal molecules. EVs are secreted by almost all cell types, including stem/progenitor cells. The EVs derived from stem/progenitor cells are analogous to the parental cells and inhibit or enhance immune response. This review aims to provide its readers a comprehensive overview of the possible mechanisms underlying the immunomodulatory effects exerted by stem/progenitor cell-derived EVs upon natural killer (NK) cells, dendritic cells (DCs), monocytes/macrophages, microglia, T cells, and B cells.

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Section: Microgliamentioning

confidence: 99%

Immunoregulatory Effects of Stem Cell-Derived Extracellular Vesicles on Immune Cells

Xie

Wang²,

She

et al. 2020

Front. Immunol.

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“…Macrophages play an important role in EAE and infiltrate the CNS during the early stages of disease (Chu et al, 2018). Given the ability of macrophages to secrete pro-inflammatory cytokines (Stow, Low, Offenhauser, & Sangermani, 2009), we examined the spinal cords of all treatment groups for macrophages, using the marker CD68, and hnRNP A1 mislocalization to determine if there was a correlation.…”

Section: Hnrnp A1 Mislocalization In Spinal Cord Gray Matter Neuronmentioning

confidence: 99%

Dysfunctional RNA‐binding protein biology and neurodegeneration in experimental autoimmune encephalomyelitis in female mice

Salapa

Libner

Levin

2019

J of Neuroscience Research

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Altered stress granule (SG) and RNA-binding protein (RBP) biology have been shown to contribute to the pathogenesis of several neurodegenerative diseases, yet little is known about their role in multiple sclerosis (MS). Pathological features associated with dysfunctional RBPs include RBP mislocalization from its normal nuclear location to the cytoplasm and the formation of chronic SGs. We tested the hypothesis that altered SG and RBP biology might contribute to the neurodegeneration in experimental autoimmune encephalomyelitis (EAE). C57BL/6 female mice were actively immunized with MOG 35-55 to induce EAE. Spinal cords were examined for mislocalization of the RBPs, heterogeneous nuclear ribonucleoprotein A1 (hnRNP A1) and TAR-DNA binding protein-43 (TDP-43), SGs, neurodegeneration (SMI-32), T cells (CD3), and macrophages (CD68). In contrast to naive mice, mice with EAE showed SG formation (p < 0.0001) and mislocalization of hnRNP A1 (p < 0.05) in neurons of the ventral spinal cord gray matter, which correlated with clinical score (R = 0.8104, p = 0.0253). In these same areas, there was a neuronal loss (p < 0.0001) and increased SMI-32 immunoreactivity (both markers of neurodegeneration) and increased staining for CD3 + T cells and IFN-gamma. These findings recapitulate the SG and RBP biology and markers of neurodegeneration in MS tissues and suggest that altered SG and RBP biology contribute to the neurodegeneration in EAE, which might also apply to the pathogenesis of MS.

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“…The markers of M1 and M2 polarized microglia in human glioblastoma and surrounding normal parenchyma for therapeutic use are iNOS and CD163 for M1 and Arg-1 for M2, although there was no significant correlation that was reported between these markers and patient survival time [67]. In some brain diseases, M1 macrophage polarization is activated rapidly, may be right after 6 h during the acute phase, and normally induces neuronal toxicity, tissue damage, demyelination, or even neuronal death with a large amount of pro-inflammatory cytokines released, with M2 gradually increasing until reaching the peak of disease and functionally promoting phagocytosis, Th2 and regulatory T cell differentiation, dampening Th1 cell activity, and accelerating tissue repair, majorly for long term recovery from 1 day to 14 days or longer [68]. For instance, it was proposed by Mi et al (2018) that shifting of M1 microglial from M2 occurred when developing stress-induced hypertension in a rat model, although M2 markers were found to be higher during the early stage of disease development [69].…”

Section: Role Of Macrophages In Brain Injuries and Neuron Protectionmentioning

confidence: 99%

Chemopreventive Effects of Phytochemicals and Medicines on M1/M2 Polarized Macrophage Role in Inflammation-Related Diseases

Koh

Yang

Lai

et al. 2018

IJMS

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Macrophages can polarize into two different states (M1 and M2), which play contrasting roles during pathogenesis or tissue damage. M1 polarized macrophages produce pro-inflammatory cytokines and mediators resulting in inflammation, while M2 macrophages have an anti-inflammatory effect. Secretion of appropriate cytokines and chemokines from macrophages can lead to the modification of the microenvironment for bridging innate and adaptive immune responses. Increasing evidence suggests that polarized macrophages are pivotal for disease progression, and the regulation of macrophage polarization may provide a new approach in therapeutic treatment of inflammation-related diseases, including cancer, obesity and metabolic diseases, fibrosis in organs, brain damage and neuron injuries, and colorectal disease. Polarized macrophages affect the microenvironment by secreting cytokines and chemokines while cytokines or mediators that are produced by resident cells or tissues may also influence macrophages behavior. The interplay of macrophages and other cells can affect disease progression, and therefore, understanding the activation of macrophages and the interaction between polarized macrophages and disease progression is imperative prior to taking therapeutic or preventive actions. Manipulation of macrophages can be an entry point for disease improvement, but the mechanism and potential must be understood. In this review, some advanced studies regarding the role of macrophages in different diseases, potential mechanisms involved, and intervention of drugs or phytochemicals, which are effective on macrophage polarization, will be discussed.

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The roles of macrophages and microglia in multiple sclerosis and experimental autoimmune encephalomyelitis

Cited by 259 publications

References 89 publications

Immunoregulatory Effects of Stem Cell-Derived Extracellular Vesicles on Immune Cells

Immunoregulatory Effects of Stem Cell-Derived Extracellular Vesicles on Immune Cells

Dysfunctional RNA‐binding protein biology and neurodegeneration in experimental autoimmune encephalomyelitis in female mice

Chemopreventive Effects of Phytochemicals and Medicines on M1/M2 Polarized Macrophage Role in Inflammation-Related Diseases

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