| pubmed-article:8985346 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8985346 | lifeskim:mentions | umls-concept:C0010823 | lld:lifeskim |
| pubmed-article:8985346 | lifeskim:mentions | umls-concept:C0877837 | lld:lifeskim |
| pubmed-article:8985346 | lifeskim:mentions | umls-concept:C0022688 | lld:lifeskim |
| pubmed-article:8985346 | lifeskim:mentions | umls-concept:C2587213 | lld:lifeskim |
| pubmed-article:8985346 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
| pubmed-article:8985346 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:8985346 | pubmed:dateCreated | 1997-1-31 | lld:pubmed |
| pubmed-article:8985346 | pubmed:abstractText | Antiviral mechanisms by which natural killer (NK) cells control murine cytomegalovirus (MCMV) infection in the spleens and livers of C57BL/6 mice were measured, revealing different mechanisms of control in different organs. Three days postinfection, MCMV titers in the spleens of perforin 0/0 mice were higher than in those of perforin +/+ mice, but no elevation of liver titers was found in perforin 0/0 mice. NK cell depletion in MCMV-infected perforin 0/0 mice resulted only in an increase in liver viral titers and not in spleen titers. Depletion of gamma interferon (IFN-gamma) in C57BL/6 mice by injections with monoclonal antibodies to IFN-gamma resulted in an increase of viral titers in the liver but not in the spleen. Analyses using IFN-gamma-receptor-deficient mice, rendered chimeric with C57BL/6 bone marrow cells, indicated that in a recipient environment where IFN-gamma cannot exert its effects, the depletion of NK cells caused an increase in MCMV titers in the spleens but had little effect in the liver. IFN-gamma has the ability to induce a variety of cells to produce nitric oxide, and administrating the nitric oxide synthase inhibitor N(omega)-monomethyl-L-arginine into MCMV-infected C57BL/6 mice resulted in MCMV titer increases in the liver but not in the spleen. Taken together, these data suggest that in C57BL/6 mice, there is a dichotomy in the mechanisms utilized by NK cells in the regulation of MCMV in different organs. In the spleen NK cells exert their effects in a perforin-dependent manner, suggesting a cytotoxic mechanism, while in the liver the production of IFN-gamma by NK cells may be a predominant mechanism in the regulation of MCMV synthesis. These results may explain why the Cmv-lr locus, which maps closely to genes regulating NK cell cytotoxic function, confers an NK cell-dependent resistance to MCMV infection in the spleen but not in the liver. | lld:pubmed |
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| pubmed-article:8985346 | pubmed:language | eng | lld:pubmed |
| pubmed-article:8985346 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8985346 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:8985346 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8985346 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:8985346 | pubmed:issn | 0022-538X | lld:pubmed |
| pubmed-article:8985346 | pubmed:author | pubmed-author:WelshR MRM | lld:pubmed |
| pubmed-article:8985346 | pubmed:author | pubmed-author:TanC CCC | lld:pubmed |
| pubmed-article:8985346 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8985346 | pubmed:volume | 71 | lld:pubmed |
| pubmed-article:8985346 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8985346 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8985346 | pubmed:pagination | 267-75 | lld:pubmed |
| pubmed-article:8985346 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:8985346 | pubmed:year | 1997 | lld:pubmed |
| pubmed-article:8985346 | pubmed:articleTitle | Distinct organ-dependent mechanisms for the control of murine cytomegalovirus infection by natural killer cells. | lld:pubmed |
| pubmed-article:8985346 | pubmed:affiliation | Department of Pathology, University of Massachusetts Medical Center, Worcester 01655, USA. | lld:pubmed |
| pubmed-article:8985346 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:8985346 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
