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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5
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pubmed:dateCreated |
1982-5-21
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pubmed:abstractText |
An H-2Db heterozygous tumor cell line and a variant subclone bearing a mutant gene product were used to analyze the H-2Db specificity of cytotoxic T lymphocytes (CTL) generated during a Moloney murine sarcoma virus (MSV) infection. When the mutant cells were used as targets for MSV-specific CTL, the amount of cell lysis, compared with that seen with the nonmutant parental cells, was drastically decreased. However, cells of the mutant clones remained susceptible to allogeneic CTL specific for the nonmutant H-2Db molecule. The mutant cells also did not differ from the parent cells in their level of viral antigen expression. Biochemically the parental and mutant molecules were similar but not identical. The data indicate that minor alterations of the H-2 antigens caused by somatic mutation may prevent virus-infected cells from being recognized as targets by CTL.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:issn |
0093-7711
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
14
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
429-36
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:6174439-Animals,
pubmed-meshheading:6174439-Cytotoxicity, Immunologic,
pubmed-meshheading:6174439-Epitopes,
pubmed-meshheading:6174439-Female,
pubmed-meshheading:6174439-H-2 Antigens,
pubmed-meshheading:6174439-Hybridomas,
pubmed-meshheading:6174439-Leukemia, Experimental,
pubmed-meshheading:6174439-Mice,
pubmed-meshheading:6174439-Mice, Inbred BALB C,
pubmed-meshheading:6174439-Moloney murine leukemia virus,
pubmed-meshheading:6174439-Mutation,
pubmed-meshheading:6174439-T-Lymphocytes
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pubmed:year |
1981
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pubmed:articleTitle |
Use of hybridoma-resident variant cell lines to study H-2Db/FMR-specific cytotoxic T cells.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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