Pathogenicity of antigenic variants of murine coronavirus JHM selected with monoclonal antibodies
about
Regulatory T cells in arterivirus and coronavirus infections: do they protect against disease or enhance it?Vaccination against lethal coronavirus-induced encephalitis with a synthetic decapeptide homologous to a domain in the predicted peplomer stalkA pregnancy-specific glycoprotein is expressed in the brain and serves as a receptor for mouse hepatitis virusRNase L mediated protection from virus induced demyelination.PKR mediated regulation of inflammation and IL-10 during viral encephalomyelitis.De novo recruitment of antigen-experienced and naive T cells contributes to the long-term maintenance of antiviral T cell populations in the persistently infected central nervous systemPathogenesis of chimeric MHV4/MHV-A59 recombinant viruses: the murine coronavirus spike protein is a major determinant of neurovirulence.Gamma interferon signaling in oligodendrocytes is critical for protection from neurotropic coronavirus infectionMouse hepatitis virus utilizes two carcinoembryonic antigens as alternative receptorsVirus-specific and bystander CD8 T cells recruited during virus-induced encephalomyelitisExpression of matrix metalloproteinases and their tissue inhibitor during viral encephalitis.Murine coronavirus-induced subacute fatal peritonitis in C57BL/6 mice deficient in gamma interferon.Targeted recombination within the spike gene of murine coronavirus mouse hepatitis virus-A59: Q159 is a determinant of hepatotropism.IL-27 limits central nervous system viral clearance by promoting IL-10 and enhances demyelination.Contributions of Fas-Fas ligand interactions to the pathogenesis of mouse hepatitis virus in the central nervous system.Coronavirus-induced demyelination occurs in the absence of inducible nitric oxide synthaseRole of viral persistence in retaining CD8(+) T cells within the central nervous systemMacrophage infiltration, but not apoptosis, is correlated with immune-mediated demyelination following murine infection with a neurotropic coronavirus.Monocytes regulate T cell migration through the glia limitans during acute viral encephalitis.Axonal damage is T cell mediated and occurs concomitantly with demyelination in mice infected with a neurotropic coronavirus.Murine coronavirus spike protein determines the ability of the virus to replicate in the liver and cause hepatitis.Contributions of the viral genetic background and a single amino acid substitution in an immunodominant CD8+ T-cell epitope to murine coronavirus neurovirulence.A severe acute respiratory syndrome-associated coronavirus-specific protein enhances virulence of an attenuated murine coronavirusVirus-specific regulatory T cells ameliorate encephalitis by repressing effector T cell functions from priming to effector stagesTarget-dependent B7-H1 regulation contributes to clearance of central nervous system infection and dampens morbidity.Pathogenesis of murine coronavirus in the central nervous system.Cell replacement therapies to promote remyelination in a viral model of demyelinationProgression from IgD+ IgM+ to isotype-switched B cells is site specific during coronavirus-induced encephalomyelitis.Matrix metalloproteinase expression correlates with virulence following neurotropic mouse hepatitis virus infectionRNA recombination of coronaviruses: localization of neutralizing epitopes and neuropathogenic determinants on the carboxyl terminus of peplomers.Kinetics of virus-specific CD8+ -T-cell expansion and trafficking following central nervous system infection.Promoting remyelination: utilizing a viral model of demyelination to assess cell-based therapiesControl of central nervous system viral persistence by neutralizing antibody.Shifting hierarchies of interleukin-10-producing T cell populations in the central nervous system during acute and persistent viral encephalomyelitis.CXCR3-dependent plasma blast migration to the central nervous system during viral encephalomyelitis.Virally expressed interleukin-10 ameliorates acute encephalomyelitis and chronic demyelination in coronavirus-infected mice.Inhibition of interferon-gamma signaling in oligodendroglia delays coronavirus clearance without altering demyelination.Expression of the mouse hepatitis virus receptor by central nervous system microgliaIFN-γ- and IL-10-expressing virus epitope-specific Foxp3(+) T reg cells in the central nervous system during encephalomyelitis.Enhanced antiviral T cell function in the absence of B7-H1 is insufficient to prevent persistence but exacerbates axonal bystander damage during viral encephalomyelitis.
P2860
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P2860
Pathogenicity of antigenic variants of murine coronavirus JHM selected with monoclonal antibodies
description
1986 nî lūn-bûn
@nan
1986年の論文
@ja
1986年論文
@yue
1986年論文
@zh-hant
1986年論文
@zh-hk
1986年論文
@zh-mo
1986年論文
@zh-tw
1986年论文
@wuu
1986年论文
@zh
1986年论文
@zh-cn
name
Pathogenicity of antigenic var ...... ted with monoclonal antibodies
@en
type
label
Pathogenicity of antigenic var ...... ted with monoclonal antibodies
@en
prefLabel
Pathogenicity of antigenic var ...... ted with monoclonal antibodies
@en
P2093
P2860
P1433
P1476
Pathogenicity of antigenic var ...... ted with monoclonal antibodies
@en
P2093
F A el-Zaatari
J O Fleming
L P Weiner
M D Trousdale
S A Stohlman
P2860
P304
P407
P577
1986-06-01T00:00:00Z