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Predicate | Object |
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rdf:type | |
lifeskim:mentions |
umls-concept:C0004083,
umls-concept:C0017262,
umls-concept:C0017355,
umls-concept:C0021747,
umls-concept:C0036667,
umls-concept:C0087111,
umls-concept:C0185117,
umls-concept:C0205216,
umls-concept:C0205217,
umls-concept:C0205419,
umls-concept:C0312418,
umls-concept:C0439799,
umls-concept:C1515655,
umls-concept:C1709474,
umls-concept:C2911684
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pubmed:issue |
6
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pubmed:dateCreated |
1985-12-23
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pubmed:abstractText |
Two H-2 negative variants of the YAC-1 lymphoma were selected by mutagenization and sequential in vitro selections and compared with wild-type cells for changes in NK sensitivity and H-2 expression after interferon treatment or in vivo passage. The H-2 negative variants and the low H-2 expressor YAC-1 wild-type cells had similar NK sensitivity. However, IFN-beta or recombinant IFN-gamma pretreatments increased the H-2 expression of YAC-1 and protected them from NK lysis, whereas the H-2 variants, which remained H-2 negative, were not protected and often more sensitive to NK lysis. The H-2 variants were similarly susceptible as wild-type cells to three other cellular effects of interferon: protection from virus infection, modulation of Con A capping, and inhibition of cell proliferation. Thus, the only interferon-mediated effect that distinguished the H-2 negative variants from wild-type cells was the inability of the former to increase their H-2 expression and decrease their NK sensitivity. The wild-type YAC-1 line showed increased H-2 expression and decreased NK sensitivity after in vivo passage. In contrast, in vivo passaged H-2 variants showed no reexpression of H-2, and remained NK sensitive. The altered responses to interferon and in vivo passage were specific for loss or down-regulation of H-2, because Thy-1 loss (H-2 positive) YAC-1 variants behaved as the wild-type cells in all respects. This study supports the hypothesis that NK cells may function in vivo to eliminate host cells that fail to express H-2 after interferon stimulation during an immune response; such cells are a potential threat because they may escape recognition by T lymphocytes despite the expression of viral or tumor-associated antigens.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0022-1767
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
135
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
4281-8
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:3905967-Animals,
pubmed-meshheading:3905967-Antilymphocyte Serum,
pubmed-meshheading:3905967-Cell Line,
pubmed-meshheading:3905967-Cytotoxicity, Immunologic,
pubmed-meshheading:3905967-Genetic Variation,
pubmed-meshheading:3905967-H-2 Antigens,
pubmed-meshheading:3905967-Interferon Type I,
pubmed-meshheading:3905967-Killer Cells, Natural,
pubmed-meshheading:3905967-Mice,
pubmed-meshheading:3905967-Neoplasm Transplantation,
pubmed-meshheading:3905967-T-Lymphocytes, Cytotoxic,
pubmed-meshheading:3905967-beta 2-Microglobulin
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pubmed:year |
1985
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pubmed:articleTitle |
YAC-1 MHC class I variants reveal an association between decreased NK sensitivity and increased H-2 expression after interferon treatment or in vivo passage.
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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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