TNF alpha promotes proliferation of oligodendrocyte progenitors and remyelination (Q48744723)

15 February 2018

title

TNF alpha promotes proliferation of oligodendrocyte progenitors and remyelination (English)

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15 February 2018

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Arnett HA

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15 February 2018

Mason J

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15 February 2018

Marino M

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15 February 2018

Suzuki K

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15 February 2018

Matsushima GK

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15 February 2018

Ting JP

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15 February 2018

language of work or name

English

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publication date

1 November 2001

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15 February 2018

published in

Nature Neuroscience

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15 February 2018

volume

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15 February 2018

issue

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15 February 2018

page(s)

1116-1122

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15 February 2018

Endogenous Progenitors Remyelinate Demyelinated Axons in the Adult CNS

cites work

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7 January 2021

Proliferation of mature oligodendrocytes after trauma to the central nervous system

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Embryonic expression of myelin genes: evidence for a focal source of oligodendrocyte precursors in the ventricular zone of the neural tube

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A crucial role for neurotrophin-3 in oligodendrocyte development

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Origin of oligodendrocytes within the human spinal cord

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Evidence for migration of oligodendrocyte–type-2 astrocyte progenitor cells into the developing rat optic nerve

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Progenitor cells of the adult mouse subventricular zone proliferate, migrate and differentiate into oligodendrocytes after demyelination

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Delayed changes in growth factor gene expression during slow remyelination in the CNS of aged rats

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Mature oligodendrocyte apoptosis precedes IGF-1 production and oligodendrocyte progenitor accumulation and differentiation during demyelination/remyelination

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Apoptosis control by death and decoy receptors

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Cytokine regulation of secondary lymphoid organ development.

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Dual role of tumor necrosis factor alpha in brain injury

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TNF is a potent anti-inflammatory cytokine in autoimmune-mediated demyelination.

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Uncoupling the proinflammatory from the immunosuppressive properties of tumor necrosis factor (TNF) at the p55 TNF receptor level: implications for pathogenesis and therapy of autoimmune demyelination

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Increased MRI activity and immune activation in two multiple sclerosis patients treated with the monoclonal anti-tumor necrosis factor antibody cA2.

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The neurotoxicant, cuprizone, as a model to study demyelination and remyelination in the central nervous system.

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Microglial/macrophage accumulation during cuprizone-induced demyelination in C57BL/6 mice

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Gene expression in brain during cuprizone-induced demyelination and remyelination

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7 January 2021

Rapid upregulation of the Pi isoform of glutathione-S-transferase in mouse brains after withdrawal of the neurotoxicant, cuprizone

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Myelination in the absence of galactocerebroside and sulfatide: normal structure with abnormal function and regional instability.

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Monoclonal autoantibodies promote central nervous system repair in an animal model of multiple sclerosis

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Identification of autoantibodies associated with myelin damage in multiple sclerosis

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Role of lymphotoxin and the type I TNF receptor in the formation of germinal centers

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Immune and inflammatory responses in TNF alpha-deficient mice: a critical requirement for TNF alpha in the formation of primary B cell follicles, follicular dendritic cell networks and germinal centers, and in the maturation of the humoral immune re

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7 January 2021

Characterization of tumor necrosis factor-deficient mice

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Differential Oligodendroglial Expression of the Tumor Necrosis Factor Receptors In Vivo and In Vitro

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7 January 2021

Differential expression, cytokine modulation, and specific functions of type-1 and type-2 tumor necrosis factor receptors in rat glia

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7 January 2021

Tumor necrosis factor-alpha modulates the proliferation of neural progenitors in the subventricular/ventricular zone of adult rat brain

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An antibody to lymphotoxin and tumor necrosis factor prevents transfer of experimental allergic encephalomyelitis

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Critical Points of Tumor Necrosis Factor Action in Central Nervous System Autoimmune Inflammation Defined by Gene Targeting

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Gene therapy for chronic relapsing experimental allergic encephalomyelitis using cells expressing a novel soluble p75 dimeric TNF receptor

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7 January 2021

Oligodendrocyte apoptosis and primary demyelination induced by local TNF/p55TNF receptor signaling in the central nervous system of transgenic mice: models for multiple sclerosis with primary oligodendrogliopathy.

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The induction of EAE is only partially dependent on TNF receptor signaling but requires the IL-1 type I receptor.

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Interleukin-1beta promotes repair of the CNS.

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A Pi Form of Glutathione-S-Transferase Is a Myelin-and Oligodendrocyte-Associated Enzyme in Mouse Brain

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Identifiers

DOI

10.1038/NN738

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15 February 2018

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15 February 2018