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rdf:type |
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lifeskim:mentions |
umls-concept:C0021311,
umls-concept:C0035366,
umls-concept:C0039194,
umls-concept:C0039198,
umls-concept:C0085358,
umls-concept:C0205245,
umls-concept:C0205322,
umls-concept:C0684336,
umls-concept:C1332717,
umls-concept:C1413244,
umls-concept:C1706438,
umls-concept:C2698600
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pubmed:issue |
3
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pubmed:dateCreated |
2004-3-19
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pubmed:abstractText |
The establishment of viral persistence generally requires evasion of the host CD8(+) T cell response. Here we describe a form of evasion wherein the CD8(+) T cells are fully capable of recognizing their cognate antigen but their effector functions are suppressed by regulatory T cells. Virus-specific CD8(+) T cells adoptively transferred into mice persistently infected with Friend virus proliferated and appeared activated, but failed to produce IFNgamma or reduce virus loads. Cotransfer experiments revealed that a subpopulation of CD4(+) T cells from persistently infected mice suppressed IFNgamma production by the CD8(+) T cells. Treatment of persistently infected mice with anti-GITR antibody to ameliorate suppression by regulatory T cells significantly improved IFNgamma production by transferred CD8(+) T cells and allowed a significant reduction in viral loads. The results indicate that CD4(+) regulatory T cells contribute to viral persistence and demonstrate an immunotherapy for treating chronic retroviral infections.
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pubmed:commentsCorrections |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies,
http://linkedlifedata.com/resource/pubmed/chemical/Epitopes, T-Lymphocyte,
http://linkedlifedata.com/resource/pubmed/chemical/Gene Products, gag,
http://linkedlifedata.com/resource/pubmed/chemical/Glucocorticoid-Induced...,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Nerve Growth Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Tumor Necrosis Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Tnfrsf18 protein, mouse
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
1074-7613
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pubmed:author |
pubmed-author:DittmerUlfU,
pubmed-author:EvansLeonard HLH,
pubmed-author:GreenbergPhilip DPD,
pubmed-author:HasenkrugKim JKJ,
pubmed-author:HeHongH,
pubmed-author:IwashiroMichihiroM,
pubmed-author:MesserRonald JRJ,
pubmed-author:OhlenClaesC,
pubmed-author:OlbrichAnke R MAR,
pubmed-author:PetersonKarin EKE,
pubmed-author:SakaguchiShimonS,
pubmed-author:SchimmerSimoneS,
pubmed-author:StromnesIngunn MIM,
pubmed-author:YangGuojunG
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pubmed:issnType |
Print
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pubmed:volume |
20
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
293-303
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:15030773-Acute Disease,
pubmed-meshheading:15030773-Adoptive Transfer,
pubmed-meshheading:15030773-Animals,
pubmed-meshheading:15030773-Antibodies,
pubmed-meshheading:15030773-CD4-Positive T-Lymphocytes,
pubmed-meshheading:15030773-CD8-Positive T-Lymphocytes,
pubmed-meshheading:15030773-Epitopes, T-Lymphocyte,
pubmed-meshheading:15030773-Friend murine leukemia virus,
pubmed-meshheading:15030773-Gene Products, gag,
pubmed-meshheading:15030773-Glucocorticoid-Induced TNFR-Related Protein,
pubmed-meshheading:15030773-Interferon-gamma,
pubmed-meshheading:15030773-Mice,
pubmed-meshheading:15030773-Mice, Inbred C57BL,
pubmed-meshheading:15030773-Mutation,
pubmed-meshheading:15030773-Receptors, Nerve Growth Factor,
pubmed-meshheading:15030773-Receptors, Tumor Necrosis Factor,
pubmed-meshheading:15030773-Retroviridae Infections,
pubmed-meshheading:15030773-Tumor Virus Infections,
pubmed-meshheading:15030773-Virus Latency
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pubmed:year |
2004
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pubmed:articleTitle |
Functional impairment of CD8(+) T cells by regulatory T cells during persistent retroviral infection.
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pubmed:affiliation |
Institut für Virologie des Universitätsklinikums, 45122 Essen, Germany.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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