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About:
Activation of Vγ9Vδ2 T cells by non-peptidic antigens induces the inhibition of subgenomic HCV replication
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schema:ScholarlyArticle
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wasabi.inria.fr
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Type:
Academic Article
research paper
schema:ScholarlyArticle
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type
Academic Article
research paper
schema:ScholarlyArticle
isDefinedBy
Covid-on-the-Web dataset
title
Activation of Vγ9Vδ2 T cells by non-peptidic antigens induces the inhibition of subgenomic HCV replication
Creator
Agrati, Chiara
Castilletti, Concetta
Poccia, Fabrizio
Abbate, Isabella
Capobianchi, Maria
D'offizi, Gianpiero
Alonzi, Tonino
De Santis, Rafaella
Fimia, Gian
Siepi, Francesca
Tripodi, Marco
source
Medline; PMC
abstract
Hepatitis C virus (HCV) has evolved complex strategies to evade host immune responses and establish chronic infection. Since human Vγ9Vδ2 T lymphocytes play a critical role in the immune response against viruses, we analyzed their antiviral functions on Huh7 hepatoma cells carrying the subgenomic HCV replicon (Rep60 cells). In a transwell culture system, Rep60 cells were co-cultured with either PBMCs or highly purified γδ T cells stimulated by non-peptidic antigens. Vγ9Vδ2 T cell activation was associated with a dramatic reduction of HCV RNA levels. Neutralizing antibodies targeting IFN-γ revealed a critical role for this cytokine in the inhibition of HCV replication. Interestingly, drugs already in clinical use, such as Phosphostim and Zoledronate, known to activate γδ T cells, were shown to induce the inhibition of HCV replication mediated by Vγ9Vδ2 T cells of HCV patients. Our data suggest that the therapeutic activation of Vγ9Vδ2 T lymphocytes may represent an additional strategy to inhibit HCV replication and to restore a T(h)1-oriented immune response in HCV-infected patients.
has issue date
2005-12-16
(
xsd:dateTime
)
bibo:doi
10.1093/intimm/dxh337
bibo:pmid
16361319
has license
no-cc
sha1sum (hex)
b7f6ba695cb5061e51f65a134ce8dd9e9c7a5947
schema:url
https://doi.org/10.1093/intimm/dxh337
resource representing a document's title
Activation of Vγ9Vδ2 T cells by non-peptidic antigens induces the inhibition of subgenomic HCV replication
has PubMed Central identifier
PMC7109927
has PubMed identifier
16361319
schema:publication
Int Immunol
resource representing a document's body
covid:b7f6ba695cb5061e51f65a134ce8dd9e9c7a5947#body_text
is
schema:about
of
named entity 'HCV'
named entity 'activation'
named entity 'Our'
named entity 'culture system'
named entity 'HCV'
named entity 'carrying'
named entity 'cytokine'
named entity 'inhibition'
named entity 'inhibition'
covid:arg/b7f6ba695cb5061e51f65a134ce8dd9e9c7a5947
named entity 'mediated'
named entity 'replication'
named entity 'T lymphocytes'
named entity 'HCV'
named entity 'RNA'
named entity 'PBMCs'
named entity 'immune responses'
named entity 'patients'
named entity 'strategies'
named entity 'IFN'
named entity 'hepatocytes'
named entity 'cytokines'
named entity 'TNF-a'
named entity 'antiviral activity'
named entity 'Life Technologies'
named entity 'IFN'
named entity 'sodium azide'
named entity 'fetal bovine serum'
named entity 'IgG1'
named entity 'revealed'
named entity 'subgenomic'
named entity 'HCV'
named entity 'host immune responses'
named entity 'HCV'
named entity 'IFN'
named entity 'critical role'
named entity 'HCV'
named entity 'HCV'
named entity 'HCV'
named entity 'antigens'
named entity 'PBMCs'
named entity 'co-cultures'
named entity 'effector cells'
named entity 'supernatants'
named entity 'HCV'
named entity 'HCV'
named entity 'HCV'
named entity 'HCV'
named entity 'replicon'
named entity 'IFN-a'
named entity 'HCV'
named entity 'IFN'
named entity 'hepadnavirus'
named entity 'hepatoma'
named entity 'antigens'
named entity 'antiviral activity'
named entity 'complement'
named entity 'RT-PCR'
named entity 'HCV'
named entity 'IL-10'
named entity 'HCV'
named entity 'clone'
named entity 'phenotype'
named entity 'lymphocytes'
named entity 'cytokines'
named entity 'staining'
named entity 'HCV'
named entity 'co-cultures'
named entity 'microbeads'
named entity 'peptidic'
named entity 'Zoledronate'
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