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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
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pubmed:dateCreated |
1992-3-30
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pubmed:abstractText |
Three Epstein-Barr-virus-transformed lymphoblastoid cell lines (LCL) were analysed on the basis of their CD23 expression. Levels of EBV-DNA were compared in the positive and negative subpopulations. Two lines were further analysed with regard to EBNA, cytoplasmic immunoglobulin (cIg) and lytic (EA/VCA) protein expression. Both subpopulations had a similar MHC class-II transcription, but the CD23- subpopulation had a lower plating efficiency and a lower rate of DNA synthesis. In the B6, NAD50 and 0467.3 cell lines, CD23- cells contained 2 +/- 0.2 - 6.4 +/- 3.0 times less EBV DNA than the corresponding CD23+ population. EBNA was expressed in 81 +/- 4.2% - 93 +/- 3.8% of the CD23+ cells and in 0 - 46 +/- 8.0% of the CD23- cells. No CD23+ cells in B6 or NAD50 contained any EA/VCA, while 19 +/- 2.8% - 24 +/- 4.2% of the CD23- cells were positive for the lytic-cycle-associated antigens. Of the CD23- cells, 70 +/- 8.6% - 86 +/- 6.0% were positive for cytoplasmic immunoglobulin compared to 14.7 +/- 2.7% - 14.9 +/- 1.8% in the corresponding CD23+ population. We have previously shown that only 18% of the cIg-positive cells were EBNA-positive in the B6 line compared to 94% in the cIg- population. This was open to 2 alternative interpretations: loss of EBV genomes from a fraction of the cells with subsequent differentiation to secretory immunoglobulin production, or down-regulation of EBNA expression in differentiating, EBV-genome-positive cells. Our present findings speak for the first alternative, indicating that a certain proportion of the cells may lose their EBV genomes in both long-established and freshly transformed LCLs. This is accompanied by a reduced percentage of EBNA-positive cells, the disappearance of at least one activation marker (CD23) associated with the virally induced blast transformation, and an increased synthesis of cIg.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Differentiation...,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Viral,
http://linkedlifedata.com/resource/pubmed/chemical/Capsid Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Epstein-Barr Virus Nuclear Antigens,
http://linkedlifedata.com/resource/pubmed/chemical/Epstein-Barr viral capsid antigen,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Fc,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, IgE,
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 |
0020-7136
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
20
|
pubmed:volume |
50
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
589-92
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:1311286-Antibody Formation,
pubmed-meshheading:1311286-Antigens, Differentiation, B-Lymphocyte,
pubmed-meshheading:1311286-Antigens, Viral,
pubmed-meshheading:1311286-Capsid Proteins,
pubmed-meshheading:1311286-Cell Division,
pubmed-meshheading:1311286-Cells, Cultured,
pubmed-meshheading:1311286-Epstein-Barr Virus Nuclear Antigens,
pubmed-meshheading:1311286-Herpesvirus 4, Human,
pubmed-meshheading:1311286-Lymphocyte Subsets,
pubmed-meshheading:1311286-Receptors, Fc,
pubmed-meshheading:1311286-Receptors, IgE,
pubmed-meshheading:1311286-Viral Proteins,
pubmed-meshheading:1311286-Virus Replication
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pubmed:year |
1992
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pubmed:articleTitle |
Cell phenotype (CD23)-dependent variation in EBV genome copy numbers within lymphoblastoid cell lines (LCL).
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pubmed:affiliation |
Department of Medical Cell Genetics, Karolinska Institutet, Stockholm, Sweden.
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pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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