Pathological changes in the spleens of gamma interferon receptor-deficient mice infected with murine gammaherpesvirus: a role for CD8 T cells.
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The role of myeloid cell activation and arginine metabolism in the pathogenesis of virus-induced diseasesEnhanced response of T cells from murine gammaherpesvirus 68-infected mice lacking the suppressor of T cell receptor signaling molecules Sts-1 and Sts-2Natural history of murine -herpesvirus infectionInterplay of Murine Gammaherpesvirus 68 with NF-kappaB Signaling of the HostViruses in Idiopathic Pulmonary Fibrosis. Etiology and ExacerbationA novel Cre recombinase imaging system for tracking lymphotropic virus infection in vivo.Three distinct regions of the murine gammaherpesvirus 68 genome are transcriptionally active in latently infected mice.Pathogenesis of a model gammaherpesvirus in a natural hostDissecting the host response to a gamma-herpesvirus.Disruption of the murine gammaherpesvirus 68 M1 open reading frame leads to enhanced reactivation from latency.Gamma interferon (IFN-gamma) receptor null-mutant mice are more susceptible to herpes simplex virus type 1 infection than IFN-gamma ligand null-mutant miceOngoing viral replication is required for gammaherpesvirus 68-induced vascular damage.Inhibition of NF-kappaB signaling reduces virus load and gammaherpesvirus-induced pulmonary fibrosisViral latency and its regulation: lessons from the gamma-herpesviruses.gamma-Herpesvirus-induced protection against bacterial infection is transient.Maintenance of gammaherpesvirus latency requires viral cyclin in the absence of B lymphocytes.CD80 and CD86 control antiviral CD8+ T-cell function and immune surveillance of murine gammaherpesvirus 68.Postexposure vaccination massively increases the prevalence of gamma-herpesvirus-specific CD8+ T cells but confers minimal survival advantage on CD4-deficient mice.Strain-dependent requirement for IFN-γ for respiratory control and immunotherapy in murine gammaherpesvirus infectionMalignant catarrhal fever induced by Alcelaphine herpesvirus 1 is characterized by an expansion of activated CD3+CD8+CD4- T cells expressing a cytotoxic phenotype in both lymphoid and non-lymphoid tissuesEstablishment of murine gammaherpesvirus latency in B cells is not a stochastic event.CD8+ T Cell Response to Gammaherpesvirus Infection Mediates Inflammation and Fibrosis in Interferon Gamma Receptor-Deficient MiceMurine gammaherpesvirus 68 infection protects lupus-prone mice from the development of autoimmunity.CD4(+) T cell-mediated control of a gamma-herpesvirus in B cell-deficient mice is mediated by IFN-gamma.Identification of the in vivo role of a viral bcl-2Ataxia telangiectasia mutated kinase controls chronic gammaherpesvirus infection.Autophagy Genes Enhance Murine Gammaherpesvirus 68 Reactivation from Latency by Preventing Virus-Induced Systemic Inflammation.A gammaherpesvirus-secreted activator of Vbeta4+ CD8+ T cells regulates chronic infection and immunopathology.CD4 T cell responses in latent and chronic viral infections.Ablation of STAT3 in the B Cell Compartment Restricts Gammaherpesvirus Latency In Vivo.The small noncoding RNAs (sncRNAs) of murine gammaherpesvirus 68 (MHV-68) are involved in regulating the latent-to-lytic switch in vivoThe murine gammaherpesvirus 68 v-cyclin is a critical regulator of reactivation from latency.Immune control of the number and reactivation phenotype of cells latently infected with a gammaherpesvirus.The de novo methyltransferases DNMT3a and DNMT3b target the murine gammaherpesvirus immediate-early gene 50 promoter during establishment of latency.Critical role for a high-affinity chemokine-binding protein in gamma-herpesvirus-induced lethal meningitisMurine gammaherpesvirus 68 open reading frame 45 plays an essential role during the immediate-early phase of viral replication.The anti-fibrotic effect of inhibition of TGFβ-ALK5 signalling in experimental pulmonary fibrosis in mice is attenuated in the presence of concurrent γ-herpesvirus infection.Comparison of the Rta/Orf50 transactivator proteins of gamma-2-herpesviruses.Critical role of CD4 T cells in an antibody-independent mechanism of vaccination against gammaherpesvirus latency.Murine gammaherpesvirus-68 infection causes multi-organ fibrosis and alters leukocyte trafficking in interferon-gamma receptor knockout mice.
P2860
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P2860
Pathological changes in the spleens of gamma interferon receptor-deficient mice infected with murine gammaherpesvirus: a role for CD8 T cells.
description
1997 nî lūn-bûn
@nan
1997年の論文
@ja
1997年学术文章
@wuu
1997年学术文章
@zh-cn
1997年学术文章
@zh-hans
1997年学术文章
@zh-my
1997年学术文章
@zh-sg
1997年學術文章
@yue
1997年學術文章
@zh
1997年學術文章
@zh-hant
name
Pathological changes in the sp ...... virus: a role for CD8 T cells.
@en
Pathological changes in the sp ...... virus: a role for CD8 T cells.
@nl
type
label
Pathological changes in the sp ...... virus: a role for CD8 T cells.
@en
Pathological changes in the sp ...... virus: a role for CD8 T cells.
@nl
prefLabel
Pathological changes in the sp ...... virus: a role for CD8 T cells.
@en
Pathological changes in the sp ...... virus: a role for CD8 T cells.
@nl
P2093
P2860
P1433
P1476
Pathological changes in the sp ...... svirus: a role for CD8 T cells
@en
P2093
P2860
P304
P407
P577
1997-06-01T00:00:00Z