IFN-γ signaling to astrocytes protects from autoimmune mediated neurological disability - Wikidata - wikimedia - TriplyDB

IFN-γ signaling to astrocytes protects from autoimmune mediated neurological disability

IFN-γ signaling to astrocytes protects from autoimmune mediated neurological disability

http://www.wikidata.org/entity/Q34359503

about

Astrocytes in Oligodendrocyte Lineage Development and White Matter Pathology The multifaceted role of astrocytes in regulating myelination Control of autoimmune CNS inflammation by astrocytes Immune privilege as an intrinsic CNS property: astrocytes protect the CNS against T-cell-mediated neuroinflammation Neuroprotection by IFN-γ via astrocyte-secreted IL-6 in acute neuroinflammation.Chemokine receptor expression by inflammatory T cells in EAE.The contribution of immune and glial cell types in experimental autoimmune encephalomyelitis and multiple sclerosis Suppressors of cytokine signaling 1 and 3 are upregulated in brain resident cells in response to virus-induced inflammation of the central nervous system via at least two distinctive pathways.Silencing IFN-γ binding/signaling in astrocytes versus microglia leads to opposite effects on central nervous system autoimmunity.Astrocyte response to IFN-γ limits IL-6-mediated microglia activation and progressive autoimmune encephalomyelitis.Anti-inflammatory mechanisms of IFN-γ studied in experimental autoimmune encephalomyelitis reveal neutrophils as a potential target in multiple sclerosis.Sustained TNF production by central nervous system infiltrating macrophages promotes progressive autoimmune encephalomyelitis.Treatment of ongoing autoimmune encephalomyelitis with activated B-cell progenitors maturing into regulatory B cells.Loss of astrocytic leptin signaling worsens experimental autoimmune encephalomyelitis.The kinetics of myelin antigen uptake by myeloid cells in the central nervous system during experimental autoimmune encephalomyelitis Role of CD25(+) CD4(+) T cells in acute and persistent coronavirus infection of the central nervous system.Ifit2 deficiency results in uncontrolled neurotropic coronavirus replication and enhanced encephalitis via impaired alpha/beta interferon induction in macrophages.Interferons in the central nervous system: a few instruments play many tunes.Opposing Roles of Interferon-Gamma on Cells of the Central Nervous System in Autoimmune Neuroinflammation.Overview of Innovative Mouse Models for Imaging Neuroinflammation.Astrocytes: Integrative Regulators of Neuroinflammation in Stroke and Other Neurological Diseases.Cytokine networks in neuroinflammation.Dickkopf-3, a tissue-derived modulator of local T-cell responses.Astrocyte-derived retinoic acid: a novel regulator of blood-brain barrier function in multiple sclerosis.Macrophages and the Recovery from Acute and Chronic Inflammation.A Hydrogel Bridge Incorporating Immobilized Growth Factors and Neural Stem/Progenitor Cells to Treat Spinal Cord Injury.Production of IL-27 in multiple sclerosis lesions by astrocytes and myeloid cells: Modulation of local immune responses.Blockade of sustained tumor necrosis factor in a transgenic model of progressive autoimmune encephalomyelitis limits oligodendrocyte apoptosis and promotes oligodendrocyte maturation.

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IFN-γ signaling to astrocytes protects from autoimmune mediated neurological disability

http://www.wikidata.org/entity/Q34359503

description

2012 nî lūn-bûn

@nan

2012 թուականի Յուլիսին հրատարակուած գիտական յօդուած

@hyw

2012 թվականի հուլիսին հրատարակված գիտական հոդված

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2012年の論文

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2012年論文

@yue

2012年論文

@zh-hant

2012年論文

@zh-hk

2012年論文

@zh-mo

2012年論文

@zh-tw

2012年论文

@wuu

name

IFN-γ signaling to astrocytes protects from autoimmune mediated neurological disability

@ast

IFN-γ signaling to astrocytes protects from autoimmune mediated neurological disability

@en

IFN-γ signaling to astrocytes protects from autoimmune mediated neurological disability

@nl

type

label

IFN-γ signaling to astrocytes protects from autoimmune mediated neurological disability

@ast

IFN-γ signaling to astrocytes protects from autoimmune mediated neurological disability

@en

IFN-γ signaling to astrocytes protects from autoimmune mediated neurological disability

@nl

prefLabel

IFN-γ signaling to astrocytes protects from autoimmune mediated neurological disability

@ast

IFN-γ signaling to astrocytes protects from autoimmune mediated neurological disability

@en

IFN-γ signaling to astrocytes protects from autoimmune mediated neurological disability

@nl

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JOURNAL.PONE.0042088

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IFN-γ signaling to astrocytes protects from autoimmune mediated neurological disability

@en

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Carine Savarin

http://www.w3.org/2001/XMLSchema#string

Claudia Hindinger

http://www.w3.org/2001/XMLSchema#string

Cornelia C Bergmann

http://www.w3.org/2001/XMLSchema#string

David R Hinton

http://www.w3.org/2001/XMLSchema#string

Gabriel I Parra

http://www.w3.org/2001/XMLSchema#string

Roscoe D Atkinson

http://www.w3.org/2001/XMLSchema#string

Shabbir Hussain

http://www.w3.org/2001/XMLSchema#string

Stephen A Stohlman

http://www.w3.org/2001/XMLSchema#string

Timothy W Phares

http://www.w3.org/2001/XMLSchema#string

P2860

Astrocytes: biology and pathology

Axonal plasticity and functional recovery after spinal cord injury in mice deficient in both glial fibrillary acidic protein and vimentin genes.

Regeneration beyond the glial scar

Reactive astrocytes protect tissue and preserve function after spinal cord injury

Astrocytes are active players in cerebral innate immunity

Autoimmune T cell responses in the central nervous system

SOCS1 and SOCS3 in the control of CNS immunity

Leukocyte infiltration, neuronal degeneration, and neurite outgrowth after ablation of scar-forming, reactive astrocytes in adult transgenic mice.

TNFR1 signalling is critical for the development of demyelination and the limitation of T-cell responses during immune-mediated CNS disease.

TNFα and IFNγ synergistically enhance transcriptional activation of CXCL10 in human airway smooth muscle cells via STAT-1, NF-κB, and the transcriptional coactivator CREB-binding protein.

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e42088

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scholarly article

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10.1371/JOURNAL.PONE.0042088

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22848713

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3407093

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