Role of Natural Killer Cells in the Generation of Influenza Virus-Specific Cytotoxic T Cells
Identifieur interne : 001140 ( Istex/Curation ); précédent : 001139; suivant : 001141Role of Natural Killer Cells in the Generation of Influenza Virus-Specific Cytotoxic T Cells
Auteurs : Ferdynand J. Kos ; Edgar G. EnglemanSource :
- Cellular Immunology [ 0008-8749 ] ; 1996.
English descriptors
- Teeft :
- Academic press, Accessory signals, Adherent pbmc, Assay, Autologous pbmc, Cell activation, Cell activity, Cell immuno, Cell immuno interactions, Cell responses, Critical accessory cells, Culture conditions, Cytolytic, Cytolytic activity, Cytometric analysis, Cytotoxicity assay, Days cytolytic activity, Early studies, Effector, Effector cells, Engleman, Gradient centrifugation, Human pbmc, Immunol, Immunomagnetic separation, Lysis, Melanoma cells, Mouse splenocytes, Natural killer, Palo alto, Pbmc, Previous studies, Responder, Responder cell numbers, Secondary responses, Splenocytes, Target cells, Triplicate cultures, Virus infection, Vivo, Vivo depletion.
Abstract
Abstract: Recently we reported that natural killer (NK) cells are critical accessory cells required for the differentiation of alloantigen-stimulated CD8+T cells into effector cytotoxic T lymphocytes (CTL)in vitro.In this study we provide evidence that NK cells are also required for the generation of influenza virus-specific CTL. Depletion of NK cells from responder human peripheral blood mononuclear cells or mouse splenocytes abolished the induction of influenza A virus-specific CTL under culture conditions. Treatment of C57BL/6 mice with the NK cell-depleting NK1.1 monoclonal antibody (mAb) before primary or secondary immunization with influenza A virus abrogated the capacity of CTL precursors to differentiate into influenza virus-specific CTL effectorsin vivo.These results extend our previous findings and demonstrate that NK cells critically influence the induction of antigen-specific CTL, bothin vitroandin vivo.
Url:
DOI: 10.1006/cimm.1996.0245
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Ferdynand J. Kos<affiliation><mods:affiliation>Department of Pathology, Stanford University School of Medicine, 800 Welch Road, Palo Alto, California, 94304</mods:affiliation><wicri:noCountry code="subField">94304</wicri:noCountry></affiliation><affiliation><mods:affiliation>Department of Pathology, Stanford University School of Medicine, 800 Welch Road, Palo Alto, California, 94304</mods:affiliation><wicri:noCountry code="subField">94304</wicri:noCountry></affiliation>Le document en format XML
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Kos</name><affiliation><mods:affiliation>Department of Pathology, Stanford University School of Medicine, 800 Welch Road, Palo Alto, California, 94304</mods:affiliation><wicri:noCountry code="subField">94304</wicri:noCountry></affiliation></author><author><name sortKey="Engleman, Edgar G" sort="Engleman, Edgar G" uniqKey="Engleman E" first="Edgar G." last="Engleman">Edgar G. Engleman</name><affiliation><mods:affiliation>Department of Pathology, Stanford University School of Medicine, 800 Welch Road, Palo Alto, California, 94304</mods:affiliation><wicri:noCountry code="subField">94304</wicri:noCountry></affiliation></author></analytic><monogr></monogr><series><title level="j">Cellular Immunology</title><title level="j" type="abbrev">YCIMM</title><idno type="ISSN">0008-8749</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1996">1996</date><biblScope unit="volume">173</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="1">1</biblScope><biblScope unit="page" to="6">6</biblScope></imprint><idno type="ISSN">0008-8749</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0008-8749</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Academic press</term><term>Accessory signals</term><term>Adherent pbmc</term><term>Assay</term><term>Autologous pbmc</term><term>Cell activation</term><term>Cell activity</term><term>Cell immuno</term><term>Cell immuno interactions</term><term>Cell responses</term><term>Critical accessory cells</term><term>Culture conditions</term><term>Cytolytic</term><term>Cytolytic activity</term><term>Cytometric analysis</term><term>Cytotoxicity assay</term><term>Days cytolytic activity</term><term>Early studies</term><term>Effector</term><term>Effector cells</term><term>Engleman</term><term>Gradient centrifugation</term><term>Human pbmc</term><term>Immunol</term><term>Immunomagnetic separation</term><term>Lysis</term><term>Melanoma cells</term><term>Mouse splenocytes</term><term>Natural killer</term><term>Palo alto</term><term>Pbmc</term><term>Previous studies</term><term>Responder</term><term>Responder cell numbers</term><term>Secondary responses</term><term>Splenocytes</term><term>Target cells</term><term>Triplicate cultures</term><term>Virus infection</term><term>Vivo</term><term>Vivo depletion</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: Recently we reported that natural killer (NK) cells are critical accessory cells required for the differentiation of alloantigen-stimulated CD8+T cells into effector cytotoxic T lymphocytes (CTL)in vitro.In this study we provide evidence that NK cells are also required for the generation of influenza virus-specific CTL. Depletion of NK cells from responder human peripheral blood mononuclear cells or mouse splenocytes abolished the induction of influenza A virus-specific CTL under culture conditions. Treatment of C57BL/6 mice with the NK cell-depleting NK1.1 monoclonal antibody (mAb) before primary or secondary immunization with influenza A virus abrogated the capacity of CTL precursors to differentiate into influenza virus-specific CTL effectorsin vivo.These results extend our previous findings and demonstrate that NK cells critically influence the induction of antigen-specific CTL, bothin vitroandin vivo.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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