Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1995-2-16
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.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
154
pubmed:geneSymbol
BZLF-1, EBNA-2, RAZ
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1440-9
pubmed:dateRevised
2007-11-14
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
pubmed:year
1995
pubmed:articleTitle
Activation of human thymocytes after infection by EBV.
pubmed:affiliation
Department of Pediatrics, National Jewish Center for Immunology and Respiratory Medicine, Denver, CO 80206.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't