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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
1992-8-11
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pubmed:abstractText |
The resistance of mice to lethal infection by murine CMV (MCMV) is under complex host genetic control with contributions from both H-2 and non-H-2 genes. We have previously shown that an autosomal, non-MHC encoded gene, Cmv-1, controls MCMV replication in the spleen. We have investigated the mechanism by which the Cmv-1 resistance gene confers protection against MCMV infection. Using H-2 compatible irradiation bone marrow chimeras, the enhanced resistance to MCMV infection that is associated with the Cmv-1l allele in the C57BL background was shown to be mediated by an irradiation-sensitive bone marrow-derived cell population, or a factor produced by these cells. The lack of correlation between serum IFN titers and the strain distribution pattern of Cmv-1 in CXB recombinant inbred mouse strains suggests that IFN does not mediate resistance conferred by this gene. Similarly, the lack of effect of in vivo depletion of mature CD4+ and CD8+ T cells on virus replication in C57BL/6J mice indicates that T cells are unlikely to be involved. In contrast, in vivo depletion of NK cells by injection of the anti-NK1.1 mAb PK136 abrogated restricted splenic virus replication in C57BL/6J----BALB.B chimeric mice and in the Cmv-1l CXB strains. These data indicate that the effect of the Cmv-1 gene is mediated by NK cells. The significant augmentation in NK cell activity after MCMV infection of the susceptible Cmv-1h strains (BALB/cBy), CXBG/By, CXBH/By, CXBI/By, and CXBK/By) indicates the existence in these mice of NK cells that are functionally and phenotypically distinct from those in Cmv-1l strains. NK cells present in the Cmv-1h strains are unable to restrict efficiently splenic MCMV replication in vivo, possibly due to a lack of specificity for virus-infected target cells. Finally, flow cytometric analysis of NK1-1 expression in CXB and BXD RI mice together with MCMV replication studies in the BXD RI strains indicate that Cmv-1 is closely linked to NK1.1 and other loci that reside on a distal segment of murine chromosome 6 in a region that has recently been defined as the natural killer complex.
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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 |
Jul
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pubmed:issn |
0022-1767
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
149
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pubmed:geneSymbol |
cmv-1
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
581-9
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:1378069-Animals,
pubmed-meshheading:1378069-Chromosome Mapping,
pubmed-meshheading:1378069-Cytomegalovirus Infections,
pubmed-meshheading:1378069-Female,
pubmed-meshheading:1378069-Genes,
pubmed-meshheading:1378069-Interferons,
pubmed-meshheading:1378069-Killer Cells, Natural,
pubmed-meshheading:1378069-Lymphocyte Depletion,
pubmed-meshheading:1378069-Mice,
pubmed-meshheading:1378069-Mice, Inbred BALB C,
pubmed-meshheading:1378069-Mice, Inbred C57BL,
pubmed-meshheading:1378069-Spleen,
pubmed-meshheading:1378069-Virus Replication
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pubmed:year |
1992
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pubmed:articleTitle |
The effect of the Cmv-1 resistance gene, which is linked to the natural killer cell gene complex, is mediated by natural killer cells.
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pubmed:affiliation |
Department of Microbiology, University of Western Australia, Queen Elizabeth II Medical Centre, Nedlands.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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