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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
1995-2-16
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pubmed:abstractText |
The discovery of EBV in certain T cell malignancies and the expression of the EBV receptor, CR2/CD21, on a population of immature thymocytes, T lymphoblastoid cell lines, and childhood acute T lymphoblastic leukemia cells suggested that EBV-receptor interactions on T cells may be of importance. We have shown that, within the thymus, a population of large, immature cells expresses CD21. EBV altered the activation responses of immature thymocytes in vitro. Triggering through CD2 is mitogenic for mature, but not immature, T cells. However, during infection by EBV, ligation of CD2 caused thymocytes to proliferate in the absence of exogenous cytokines. This function was a result of the interaction of EBV with its receptor, CD21, but was caused by infection rather than surface signaling, because neither specific mAb nor the P3HR-1 strain of virus mimicked the effect of B95-8. Immature thymocytes were infected by EBV, as determined by the internalization of the viral genome and its transcriptional activity. Consistent with the activity of B95-8, EBNA-2 transcripts were identified within infected thymocyte populations. In addition, components of the viral replicative pathway were expressed during infection of thymocytes. These components included transcription of BZLF-1, an early gene that characterizes EBV-infected B cells after disruption of latency. A second transcript was identified as encoding the recently characterized RAZ, which also is associated with replicative infection. The consequences of EBV infection of T cells at an early stage of differentiation may lead to failure of normal T cell repertoire development, autoimmunity, or malignancy.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Viral,
http://linkedlifedata.com/resource/pubmed/chemical/BZLF1 protein, Herpesvirus 4, Human,
http://linkedlifedata.com/resource/pubmed/chemical/DNA, Viral,
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Epstein-Barr Virus Nuclear Antigens,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Complement 3d,
http://linkedlifedata.com/resource/pubmed/chemical/Trans-Activators,
http://linkedlifedata.com/resource/pubmed/chemical/Viral Proteins
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0022-1767
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
154
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pubmed:geneSymbol |
BZLF-1,
EBNA-2,
RAZ
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1440-9
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:7822809-Antigens, Viral,
pubmed-meshheading:7822809-Base Sequence,
pubmed-meshheading:7822809-Blotting, Southern,
pubmed-meshheading:7822809-Cells, Cultured,
pubmed-meshheading:7822809-Child, Preschool,
pubmed-meshheading:7822809-DNA, Viral,
pubmed-meshheading:7822809-DNA Replication,
pubmed-meshheading:7822809-DNA-Binding Proteins,
pubmed-meshheading:7822809-Epstein-Barr Virus Nuclear Antigens,
pubmed-meshheading:7822809-Herpesviridae Infections,
pubmed-meshheading:7822809-Herpesvirus 4, Human,
pubmed-meshheading:7822809-Humans,
pubmed-meshheading:7822809-Infant,
pubmed-meshheading:7822809-Lymphocyte Activation,
pubmed-meshheading:7822809-Molecular Sequence Data,
pubmed-meshheading:7822809-Receptors, Complement 3d,
pubmed-meshheading:7822809-T-Lymphocytes,
pubmed-meshheading:7822809-Thymus Gland,
pubmed-meshheading:7822809-Trans-Activators,
pubmed-meshheading:7822809-Tumor Virus Infections,
pubmed-meshheading:7822809-Viral Proteins
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pubmed:year |
1995
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pubmed:articleTitle |
Activation of human thymocytes after infection by EBV.
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pubmed:affiliation |
Department of Pediatrics, National Jewish Center for Immunology and Respiratory Medicine, Denver, CO 80206.
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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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