Differential tumor necrosis factor receptor 2-mediated editing of virus-specific CD8+ effector T cells.
about
ADAMTS5 Is a Critical Regulator of Virus-Specific T Cell ImmunityDiverse heterologous primary infections radically alter immunodominance hierarchies and clinical outcomes following H7N9 influenza challenge in miceProtective memory responses are modulated by priming events prior to challenge.Consequences of immunodominant epitope deletion for minor influenza virus-specific CD8+-T-cell responses.Effector CD8+ T cells recovered from an influenza pneumonia differentiate to a state of focused gene expression.Intrinsic TNF/TNFR2 interactions fine-tune the CD8 T cell response to respiratory influenza virus infection in mice.Resistance of the target islet tissue to autoimmune destruction contributes to genetic susceptibility in Type 1 diabetes.Paired TCRαβ analysis of virus-specific CD8(+) T cells exposes diversity in a previously defined 'narrow' repertoireInfluenza and the challenge for immunology.Shedding of TNF receptor 2 by effector CD8⁺ T cells by ADAM17 is important for regulating TNF-α availability during influenza infection.Conserved T cell receptor usage in primary and recall responses to an immunodominant influenza virus nucleoprotein epitope.TNFR2 expression on non-bone marrow-derived cells is crucial for lipopolysaccharide-induced septic shock and downregulation of soluble TNFR2 level in serum.Role of tumor necrosis factor receptors in regulating CD8 T-cell responses during acute lymphocytic choriomeningitis virus infectionThe contextual role of TNFR family members in CD8(+) T-cell control of viral infections.Extrinsically derived TNF is primarily responsible for limiting antiviral CD8+ T cell response magnitude.Negative regulation of lung inflammation and immunopathology by TNF-α during acute influenza infectionRegulation of inflammation-associated olfactory neuronal death and regeneration by the type II tumor necrosis factor receptor.TNF receptor 1 mediates dendritic cell maturation and CD8 T cell response through two distinct mechanisms.Lack of prominent peptide-major histocompatibility complex features limits repertoire diversity in virus-specific CD8+ T cell populations.Visualizing CTL activity for different CD8+ effector T cells supports the idea that lower TCR/epitope avidity may be advantageous for target cell killing.
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P2860
Differential tumor necrosis factor receptor 2-mediated editing of virus-specific CD8+ effector T cells.
description
article científic
@ca
article scientifique
@fr
articolo scientifico
@it
artigo científico
@pt
bilimsel makale
@tr
scientific article published on March 2004
@en
vedecký článok
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vetenskaplig artikel
@sv
videnskabelig artikel
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vědecký článek
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name
Differential tumor necrosis fa ...... pecific CD8+ effector T cells.
@en
Differential tumor necrosis fa ...... pecific CD8+ effector T cells.
@nl
type
label
Differential tumor necrosis fa ...... pecific CD8+ effector T cells.
@en
Differential tumor necrosis fa ...... pecific CD8+ effector T cells.
@nl
prefLabel
Differential tumor necrosis fa ...... pecific CD8+ effector T cells.
@en
Differential tumor necrosis fa ...... pecific CD8+ effector T cells.
@nl
P2860
P50
P356
P1476
Differential tumor necrosis fa ...... pecific CD8+ effector T cells.
@en
P2093
Gabriela Diaz
P2860
P304
P356
10.1073/PNAS.0307347101
P407
P577
2004-03-01T00:00:00Z