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dc.contributor.authorTay, Chin Hun
dc.contributor.authorWelsh, Raymond M.
dc.contributor.authorBrutkiewicz, Randy R.
dc.date2022-08-11T08:08:49.000
dc.date.accessioned2022-08-23T16:09:22Z
dc.date.available2022-08-23T16:09:22Z
dc.date.issued1995-01-15
dc.date.submitted2009-01-13
dc.identifier.citation<p>J Immunol. 1995 Jan 15;154(2):780-9.</p>
dc.identifier.issn0022-1767 (Print)
dc.identifier.pmid7529286
dc.identifier.urihttp://hdl.handle.net/20.500.14038/32676
dc.description.abstractBecause class I MHC Ags have been implicated as modulators of target cell sensitivity to NK cell-mediated lysis, the regulation of virus infections and the fate of NK cells and their natural targets was examined in beta 2-microglobulin-deficient mice, which have defective class I MHC expression. Infections with either the NK cell-sensitive murine cytomegalovirus (MCMV) or the NK cell-resistant lymphocytic choriomeningitis virus (LCMV) significantly augmented NK cell activity in either C57BL/6 (+/+) or beta 2-microglobulin knockout (-/-) mice. Depletion of NK cells in vivo with antiserum to asialo-GM1 markedly enhanced the synthesis of MCMV but had no effect on the synthesis of LCMV in either strain of mouse. Analysis of naturally NK cell-sensitive thymocyte targets from these virus-infected -/- mice revealed no cell surface expression of class I MHC detectable by conformation-dependent or -independent Abs, but the virus infections enhanced class I expression on thymocytes from +/+ mice. The sensitivity of +/+ thymocytes to NK cell-mediated lysis was markedly reduced after in vivo poly inosinic:cytidylic and treatment or viral infection; in contrast, the sensitivity of the -/- thymocytes was significantly less affected by poly inosinic:cytidylic acid treatment or viral infection. These data indicate that the normal expression of class I MHC Ags on NK cells or their targets is not required for the antiviral functions of NK cells against a NK-sensitive virus (MCMV) nor do they protect a NK-resistant virus (LCMV) from the antiviral activity of NK cells.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=7529286&dopt=Abstract">Link to Article in PubMed</a></p>
dc.relation.urlhttp://www.jimmunol.org/content/154/2/780
dc.subjectAnimals; Cytotoxicity Tests, Immunologic; Flow Cytometry; H-2 Antigens; Herpesviridae Infections; Interferons; Killer Cells, Natural; Lymphocytic Choriomeningitis; Mice; Mice, Inbred C3H; Mice, Inbred C57BL; Mice, Knockout; Muromegalovirus; Poly I-C; beta 2-Microglobulin
dc.subjectImmunology and Infectious Disease
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleNK cell response to viral infections in beta 2-microglobulin-deficient mice
dc.typeJournal Article
dc.source.journaltitleJournal of immunology (Baltimore, Md. : 1950)
dc.source.volume154
dc.source.issue2
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/gsbs_sp/1235
dc.identifier.contextkey693145
html.description.abstract<p>Because class I MHC Ags have been implicated as modulators of target cell sensitivity to NK cell-mediated lysis, the regulation of virus infections and the fate of NK cells and their natural targets was examined in beta 2-microglobulin-deficient mice, which have defective class I MHC expression. Infections with either the NK cell-sensitive murine cytomegalovirus (MCMV) or the NK cell-resistant lymphocytic choriomeningitis virus (LCMV) significantly augmented NK cell activity in either C57BL/6 (+/+) or beta 2-microglobulin knockout (-/-) mice. Depletion of NK cells in vivo with antiserum to asialo-GM1 markedly enhanced the synthesis of MCMV but had no effect on the synthesis of LCMV in either strain of mouse. Analysis of naturally NK cell-sensitive thymocyte targets from these virus-infected -/- mice revealed no cell surface expression of class I MHC detectable by conformation-dependent or -independent Abs, but the virus infections enhanced class I expression on thymocytes from +/+ mice. The sensitivity of +/+ thymocytes to NK cell-mediated lysis was markedly reduced after in vivo poly inosinic:cytidylic and treatment or viral infection; in contrast, the sensitivity of the -/- thymocytes was significantly less affected by poly inosinic:cytidylic acid treatment or viral infection. These data indicate that the normal expression of class I MHC Ags on NK cells or their targets is not required for the antiviral functions of NK cells against a NK-sensitive virus (MCMV) nor do they protect a NK-resistant virus (LCMV) from the antiviral activity of NK cells.</p>
dc.identifier.submissionpathgsbs_sp/1235
dc.contributor.departmentDepartment of Pathology
dc.source.pages780-9
dc.contributor.studentChin Hun Tay


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