We are analyzing https://link.springer.com/article/10.1007/s00281-013-0382-8.

Title:
Microglia and macrophages of the central nervous system: the contribution of microglia priming and systemic inflammation to chronic neurodegeneration | Seminars in Immunopathology
Description:
Microglia, the resident immune cells of the central nervous system (CNS), play an important role in CNS homeostasis during development, adulthood and ageing. Their phenotype and function have been widely studied, but most studies have focused on their local interactions in the CNS. Microglia are derived from a particular developmental niche, are long-lived, locally replaced and form a significant part of the communication route between the peripheral immune system and the CNS; all these components of microglia biology contribute to maintaining homeostasis. Microglia function is tightly regulated by the CNS microenvironment, and increasing evidence suggests that disturbances, such as neurodegeneration and ageing, can have profound consequences for microglial phenotype and function. We describe the possible biological mechanisms underlying the altered threshold for microglial activation, also known as ‘microglial priming’, seen in CNS disease and ageing and consider how priming may contribute to turning immune-to-brain communication from a homeostatic pathway into a maladaptive response that contributes to symptoms and progression of diseases of the CNS.
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Keywords {🔍}

microglia, article, google, scholar, pubmed, cas, brain, cns, systemic, disease, cells, immune, inflammation, phenotype, macrophages, system, response, perry, activation, microglial, expression, neurodegeneration, role, priming, neurons, increased, chronic, challenge, mouse, lps, receptors, local, signalling, normal, ageing, evidence, cell, parenchyma, cytokines, proinflammatory, macrophage, tissue, receptor, symptoms, important, studies, regulation, inflammatory, function, homeostasis,

Topics {✒️}

heat-killed bacillus calmette-guérin anti-tumour necrosis factor-α prion-infected fcγ-deficient mice grafted bone-marrow-derived cells colony-stimulating factor receptor-1 hugh perry & jessica teeling transforming growth factor-β bacillus calmette-guérin sequestered transforming growth factor-beta1 mhc class ii induces amplified ifnalpha/beta colony-stimulating factor-1 ligand-receptor interactions regulating gene-autonomous transcriptional probability brain-derived neurotrophic factor article download pdf mediating nf-kappab activity pathogen-free laboratory conditions male donor-derived cells steroidal anti-inflammatory agents cytokine-induced acute inflammation blood-brain barrier permeability cell–cell-mediated modulation intact blood-brain barrier long-term repopulated primates privacy choices/manage cookies yolk-sac-derived cells donor bm-derived cells anti-inflammatory agents interleukin-4 low-level systemic inflammation fc receptor biology interferon-γ-mediated inflammation bone marrow hematopoiesis bone marrow transplants pro-inflammatory il-1beta long-lived cells derived predominantly anti-inflammatory phenotype yolk-sac-derived macrophages bone marrow chimeras age-related cns disorders mononuclear phagocyte system de novo synthesis adult naïve state anti-inflammatory il-10 cytokines blood-brain barrier lead pathogen-derived antigens express beta-galactosidase fc receptor ligation endotoxin-induced depressive symptoms complement-dependent manner

Questions {❓}

Galea I, Bechmann I, Perry VH (2007) What is immune privilege (not)?
If the microglia are exclusively derived from the yolk sac during development, the interesting question is raised as to how the population is subsequently maintained during life: what are the relative contributions of local proliferation and recruitment from the blood, and are these pathways similar under healthy and diseased conditions?

Schema {🗺️}

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         headline:Microglia and macrophages of the central nervous system: the contribution of microglia priming and systemic inflammation to chronic neurodegeneration
         description:Microglia, the resident immune cells of the central nervous system (CNS), play an important role in CNS homeostasis during development, adulthood and ageing. Their phenotype and function have been widely studied, but most studies have focused on their local interactions in the CNS. Microglia are derived from a particular developmental niche, are long-lived, locally replaced and form a significant part of the communication route between the peripheral immune system and the CNS; all these components of microglia biology contribute to maintaining homeostasis. Microglia function is tightly regulated by the CNS microenvironment, and increasing evidence suggests that disturbances, such as neurodegeneration and ageing, can have profound consequences for microglial phenotype and function. We describe the possible biological mechanisms underlying the altered threshold for microglial activation, also known as ‘microglial priming’, seen in CNS disease and ageing and consider how priming may contribute to turning immune-to-brain communication from a homeostatic pathway into a maladaptive response that contributes to symptoms and progression of diseases of the CNS.
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      headline:Microglia and macrophages of the central nervous system: the contribution of microglia priming and systemic inflammation to chronic neurodegeneration
      description:Microglia, the resident immune cells of the central nervous system (CNS), play an important role in CNS homeostasis during development, adulthood and ageing. Their phenotype and function have been widely studied, but most studies have focused on their local interactions in the CNS. Microglia are derived from a particular developmental niche, are long-lived, locally replaced and form a significant part of the communication route between the peripheral immune system and the CNS; all these components of microglia biology contribute to maintaining homeostasis. Microglia function is tightly regulated by the CNS microenvironment, and increasing evidence suggests that disturbances, such as neurodegeneration and ageing, can have profound consequences for microglial phenotype and function. We describe the possible biological mechanisms underlying the altered threshold for microglial activation, also known as ‘microglial priming’, seen in CNS disease and ageing and consider how priming may contribute to turning immune-to-brain communication from a homeostatic pathway into a maladaptive response that contributes to symptoms and progression of diseases of the CNS.
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