Source:http://linkedlifedata.com/resource/pubmed/id/20173023
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
6
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| pubmed:dateCreated |
2010-3-4
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| pubmed:abstractText |
Although chronic viral infections have evolved mechanisms to interfere with aspects of pathogen recognition by dendritic cells (DCs), the role that these APCs play in virus-specific T cell exhaustion is unclear. Herein we report that NS3-dependent suppression of Toll/IL-1 domain-containing adapter-inducing IFN-beta- and IFN-beta promoter stimulator-1- but not MyD88-coupled pathogen-recognition receptor-induced synthesis of proinflammatory cytokines (IL-12 and TNF-alpha) from DCs by hepatitis C virus (HCV) is a distinctive feature of a subgroup of chronically infected patients. The result is decreased CD8(+) T cell polyfunctional capacities (production of IFN-gamma, IL-2, TNF-alpha, and CD107a mobilization) that is confined to HCV specificities and that relates to the extent to which HCV inhibits DC responses in infected subjects, despite comparable plasma viral load, helper T cell environments, and inhibitory programmed death 1 receptor/ligand signals. Thus, subjects in whom pathogen-recognition receptor signaling in DCs was intact exhibited enhanced polyfunctionality (i.e., IL-2-secretion and CD107a). In addition, differences between HCV-infected patients in the ability of CD8(+) T cells to activate multiple functions in response to HCV did not apply to CD8(+) T cells specific for other immune-controlled viruses (CMV, EBV, and influenza). Our findings identify reversible virus evasion of DC-mediated innate immunity as an additional important factor that impacts the severity of polyfunctional CD8(+) T cell exhaustion during a chronic viral infection.
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| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
AIM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Surface,
http://linkedlifedata.com/resource/pubmed/chemical/Apoptosis Regulatory Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-2,
http://linkedlifedata.com/resource/pubmed/chemical/Pdcd1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Programmed Cell Death 1 Receptor,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Pattern Recognition
|
| pubmed:status |
MEDLINE
|
| pubmed:month |
Mar
|
| pubmed:issn |
1550-6606
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| pubmed:author | |
| pubmed:issnType |
Electronic
|
| pubmed:day |
15
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| pubmed:volume |
184
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
3134-44
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| pubmed:dateRevised |
2011-11-17
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| pubmed:meshHeading |
pubmed-meshheading:20173023-Antigens, Surface,
pubmed-meshheading:20173023-Apoptosis Regulatory Proteins,
pubmed-meshheading:20173023-CD8-Positive T-Lymphocytes,
pubmed-meshheading:20173023-Cell Degranulation,
pubmed-meshheading:20173023-Dendritic Cells,
pubmed-meshheading:20173023-Female,
pubmed-meshheading:20173023-Hepacivirus,
pubmed-meshheading:20173023-Hepatitis C, Chronic,
pubmed-meshheading:20173023-Humans,
pubmed-meshheading:20173023-Immunosuppression,
pubmed-meshheading:20173023-Interleukin-2,
pubmed-meshheading:20173023-Longitudinal Studies,
pubmed-meshheading:20173023-Male,
pubmed-meshheading:20173023-Middle Aged,
pubmed-meshheading:20173023-Myeloid Cells,
pubmed-meshheading:20173023-Programmed Cell Death 1 Receptor,
pubmed-meshheading:20173023-Receptors, Pattern Recognition,
pubmed-meshheading:20173023-Viral Load,
pubmed-meshheading:20173023-Virus Activation
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| pubmed:year |
2010
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| pubmed:articleTitle |
Dendritic cell inhibition is connected to exhaustion of CD8+ T cell polyfunctionality during chronic hepatitis C virus infection.
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| pubmed:affiliation |
Département de Microbiologie et Immunologie, Centre de Recherche du Centre Hospitalier de Université de Montréal, Montréal, Québec, Canada.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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