Absence of neurological deficits following extensive demyelination in a class I-deficient murine model of multiple sclerosis
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Theiler's virus infection: a model for multiple sclerosisThe pathophysiology of multiple sclerosis: the mechanisms underlying the production of symptoms and the natural history of the diseaseCD8+ T cells cause disability and axon loss in a mouse model of multiple sclerosisA single dose of neuron-binding human monoclonal antibody improves spontaneous activity in a murine model of demyelinationMajor histocompatibility complex class I molecules protect motor neurons from astrocyte-induced toxicity in amyotrophic lateral sclerosis.On the role of tumor necrosis factor and receptors in models of multiorgan failure, rheumatoid arthritis, multiple sclerosis and inflammatory bowel disease.Theiler's virus infection induces a predominant pathogenic CD4+ T cell response to RNA polymerase in susceptible SJL/J miceDifferential influence of interleukin-12 in the pathogenesis of autoimmune and virus-induced central nervous system demyelination.Progress in determining the causes and treatment of multiple sclerosis.Axonal loss results in spinal cord atrophy, electrophysiological abnormalities and neurological deficits following demyelination in a chronic inflammatory model of multiple sclerosisQuantitative assessment of neurologic deficits in a chronic progressive murine model of CNS demyelination.Absence of spontaneous central nervous system remyelination in class II-deficient mice infected with Theiler's virus.HLA-DQ polymorphism influences progression of demyelination and neurologic deficits in a viral model of multiple sclerosisDirect comparison of demyelinating disease induced by the Daniel's strain and BeAn strain of Theiler's murine encephalomyelitis virus.Quantitation of spinal cord demyelination, remyelination, atrophy, and axonal loss in a model of progressive neurologic injury.Spontaneous remyelination following extensive demyelination is associated with improved neurological function in a viral model of multiple sclerosis.CD4(+) and CD8(+) T cells make discrete contributions to demyelination and neurologic disease in a viral model of multiple sclerosisAxonal damage is T cell mediated and occurs concomitantly with demyelination in mice infected with a neurotropic coronavirus.CD8(+) T lymphocytes mediate Borna disease virus-induced immunopathology independently of perforinA critical role for virus-specific CD8(+) CTLs in protection from Theiler's virus-induced demyelination in disease-susceptible SJL mice.Rapid formation of extended processes and engagement of Theiler's virus-infected neurons by CNS-infiltrating CD8 T cells.The majority of infiltrating CD8+ T cells in the central nervous system of susceptible SJL/J mice infected with Theiler's virus are virus specific and fully functional.Transgenic expression of Theiler's murine encephalomyelitis virus genes in H-2(b) mice inhibits resistance to virus-induced demyelinationDifferences in avidity and epitope recognition of CD8(+) T cells infiltrating the central nervous systems of SJL/J mice infected with BeAn and DA strains of Theiler's murine encephalomyelitis virusTh17-biased RORγt transgenic mice become susceptible to a viral model for multiple sclerosis.Transgenic expression of viral capsid proteins predisposes to axonal injury in a murine model of multiple sclerosisThree dimensional MRI estimates of brain and spinal cord atrophy in multiple sclerosis.Quantitative ultrastructural analysis of a single spinal cord demyelinated lesion predicts total lesion load, axonal loss, and neurological dysfunction in a murine model of multiple sclerosisAxonal injury heralds virus-induced demyelination.Absence of perforin expression confers axonal protection despite demyelination.The immunodominant CD8+ T cell epitope region of Theiler's virus in resistant C57BL/6 mice is critical for anti-viral immune responses, viral persistence, and binding to the host cells.Deletion of beta-2-microglobulin ameliorates spinal cord lesion load and promotes recovery of brainstem NAA levels in a murine model of multiple sclerosisKallikrein 6 regulates early CNS demyelination in a viral model of multiple sclerosis.CD8+ T cells directed against a viral peptide contribute to loss of motor function by disrupting axonal transport in a viral model of fulminant demyelinationTargeting inflammatory demyelinating lesions to sites of Wallerian degeneration.The role of CD8+ T-cells in lesion formation and axonal dysfunction in multiple sclerosis.Inflammation, demyelination, neurodegeneration and neuroprotection in the pathogenesis of multiple sclerosisEffectors of demyelination and remyelination in the CNS: implications for multiple sclerosis.Inflammation on the mind: visualizing immunity in the central nervous system.Axons are injured by antigen-specific CD8(+) T cells through a MHC class I- and granzyme B-dependent mechanism.
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Absence of neurological deficits following extensive demyelination in a class I-deficient murine model of multiple sclerosis
description
article científic
@ca
article scientifique
@fr
articolo scientifico
@it
artigo científico
@pt
bilimsel makale
@tr
scientific article published on February 1998
@en
vedecký článok
@sk
vetenskaplig artikel
@sv
videnskabelig artikel
@da
vědecký článek
@cs
name
Absence of neurological defici ...... ne model of multiple sclerosis
@en
Absence of neurological defici ...... e model of multiple sclerosis.
@nl
type
label
Absence of neurological defici ...... ne model of multiple sclerosis
@en
Absence of neurological defici ...... e model of multiple sclerosis.
@nl
prefLabel
Absence of neurological defici ...... ne model of multiple sclerosis
@en
Absence of neurological defici ...... e model of multiple sclerosis.
@nl
P2093
P2860
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P1433
P1476
Absence of neurological defici ...... ne model of multiple sclerosis
@en
P2093
Cynthia Rivera-Quiñones
James D Schmelzer
Phillip A Low
Samuel F Hunter
P2860
P2888
P304
P356
10.1038/NM0298-187
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P577
1998-02-01T00:00:00Z