The Acquisition of Anti-Influenza Virus Activity by Macrophages
Identifieur interne : 002537 ( Main/Exploration ); précédent : 002536; suivant : 002538The Acquisition of Anti-Influenza Virus Activity by Macrophages
Auteurs : N. K. Mak [Australie] ; G. L. Ada [Australie]Source :
- Immunobiology [ 0171-2985 ] ; 1984.
English descriptors
- Teeft :
- Adherent, Adherent cells, Assay, Culture supernatants, Cytotoxic, Cytotoxic activity, Cytotoxicity, Effector, Effector cells, Further experiments, Immuno, Infectious virus, Influenza, Influenza virus, Influenza virus infection, Interferon, Interferon production, Lysis, Macrophage, Macrophage activation, Macrophage monolayers, Medical research, Normal mice, Normal spleen cells, Peritoneal, Peritoneal cavity, Peritoneal cells, Psis cells, Sendai, Sendai virus, Spleen, Spleen cells, Supernatant, Target cell, Target cells, Uninfected, Viral, Viral infection, Virus, Virus activity, Virus infection.
Abstract
Abstract: Exposure of resident peritoneal macrophages or thioglycollate-induced macrophages (TGMø) to influenza or Sendai virus-infected spleen cell culture supernatants (MAS) resulted in macrophage activation. When normal resident macrophages were used as effector cells, both infected P815 and L929 cells were lysed in the presence of MAS.MAS-activated TG-Mrø also lysed influenza virus-infected L929 cells. Histocompatibility between effector cells and target cells was not required for target cell destruction. The effector cells were plastic-adherent, phagocytic and Ia-. MAS-activated macrophages were also resistant to influenza virus infection in vitro. Both infectious and non-infectious preparations of influenza or Sendai virus preparations were effective at generating MAS. The mediator(s) which renders macrophages to become cytotoxic and resistant to infection was acid-stable, heat-labile (56°C, 30 min; or 100°C, 5 min), and the activity was neutralized by sheep antimouse type 1 interferon (IFN).
Url:
DOI: 10.1016/S0171-2985(84)80023-6
Affiliations:
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K." last="Mak">N. K. Mak</name><affiliation wicri:level="1"><country xml:lang="fr">Australie</country><wicri:regionArea>Department of Microbiology, John Curtin School of Medical Research, Australian National University, Canberra</wicri:regionArea><wicri:noRegion>Canberra</wicri:noRegion></affiliation></author><author><name sortKey="Ada, G L" sort="Ada, G L" uniqKey="Ada G" first="G. L." last="Ada">G. L. Ada</name><affiliation wicri:level="1"><country xml:lang="fr">Australie</country><wicri:regionArea>Department of Microbiology, John Curtin School of Medical Research, Australian National University, Canberra</wicri:regionArea><wicri:noRegion>Canberra</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j">Immunobiology</title><title level="j" type="abbrev">IMBIO</title><idno type="ISSN">0171-2985</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1984">1984</date><biblScope unit="volume">166</biblScope><biblScope unit="issue">4–5</biblScope><biblScope unit="page" from="458">458</biblScope><biblScope unit="page" to="472">472</biblScope></imprint><idno type="ISSN">0171-2985</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0171-2985</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Adherent</term><term>Adherent cells</term><term>Assay</term><term>Culture supernatants</term><term>Cytotoxic</term><term>Cytotoxic activity</term><term>Cytotoxicity</term><term>Effector</term><term>Effector cells</term><term>Further experiments</term><term>Immuno</term><term>Infectious virus</term><term>Influenza</term><term>Influenza virus</term><term>Influenza virus infection</term><term>Interferon</term><term>Interferon production</term><term>Lysis</term><term>Macrophage</term><term>Macrophage activation</term><term>Macrophage monolayers</term><term>Medical research</term><term>Normal mice</term><term>Normal spleen cells</term><term>Peritoneal</term><term>Peritoneal cavity</term><term>Peritoneal cells</term><term>Psis cells</term><term>Sendai</term><term>Sendai virus</term><term>Spleen</term><term>Spleen cells</term><term>Supernatant</term><term>Target cell</term><term>Target cells</term><term>Uninfected</term><term>Viral</term><term>Viral infection</term><term>Virus</term><term>Virus activity</term><term>Virus infection</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: Exposure of resident peritoneal macrophages or thioglycollate-induced macrophages (TGMø) to influenza or Sendai virus-infected spleen cell culture supernatants (MAS) resulted in macrophage activation. When normal resident macrophages were used as effector cells, both infected P815 and L929 cells were lysed in the presence of MAS.MAS-activated TG-Mrø also lysed influenza virus-infected L929 cells. Histocompatibility between effector cells and target cells was not required for target cell destruction. The effector cells were plastic-adherent, phagocytic and Ia-. MAS-activated macrophages were also resistant to influenza virus infection in vitro. Both infectious and non-infectious preparations of influenza or Sendai virus preparations were effective at generating MAS. The mediator(s) which renders macrophages to become cytotoxic and resistant to infection was acid-stable, heat-labile (56°C, 30 min; or 100°C, 5 min), and the activity was neutralized by sheep antimouse type 1 interferon (IFN).</div></front></TEI><affiliations><list><country><li>Australie</li></country></list><tree><country name="Australie"><noRegion><name sortKey="Mak, N K" sort="Mak, N K" uniqKey="Mak N" first="N. K." last="Mak">N. K. Mak</name></noRegion><name sortKey="Ada, G L" sort="Ada, G L" uniqKey="Ada G" first="G. L." last="Ada">G. L. Ada</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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