Regulation of lymphocyte proliferation after influenza virus infection of human mononuclear leukocytes
Identifieur interne : 000C54 ( Istex/Curation ); précédent : 000C53; suivant : 000C55Regulation of lymphocyte proliferation after influenza virus infection of human mononuclear leukocytes
Auteurs : Norbert J. Roberts Jr. [États-Unis] ; Joan E. Nichols [États-Unis]Source :
- Journal of Medical Virology [ 0146-6615 ] ; 1989-03.
Abstract
Previous studies demonstrated that in vitro infection with influenza A viruses altered several functions of human monocytes‐macrophages but did not detectably alter functions of human lymphocytes. However, both types of cells were infected, as determined by production and surface expression of viral antigens. In the current studies, human mononuclear leukocytes were infected in vitro and assayed for both influenza virus‐induced proliferation and mitogen (phytohemagglutinin [PHA])‐induced proliferation, as well as for ability to stimulate proliferative responses by normal autologous leukocytes. The leukocytes showed proliferation in response to the infectious virus, but concomitant depressed proliferative responses to PHA. Coculture experiments suggested suppression of PHA‐induced responses by the virus‐infected cells. However, upon coculture with fresh autologous leukocytes (without PHA stimulation), both virus‐infected macrophages and virus‐infected lymphocytes induced autologous lymphocyte proliferative responses. Altered proliferative responses to mitogen stimulation after exposure to the virus were not due to diminished interleukin‐1 production or diminished expression of HLA‐DR by monocytes‐macrophages. The expression of influenza virus antigens and resulting induction of autologous proliferative responses, combined with depressed mitogen‐induced proliferation, may be important in human antiviral defense.
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DOI: 10.1002/jmv.1890270302
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Roberts Jr.</name><affiliation wicri:level="2"><mods:affiliation>Infectious Diseases Unit, Department of Medicine, University of Rochester School of Medicine, Rochester, New York</mods:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">État de New York</region></placeName><wicri:cityArea>Infectious Diseases Unit, Department of Medicine, University of Rochester School of Medicine, Rochester</wicri:cityArea></affiliation><affiliation wicri:level="2"><mods:affiliation>Correspondence address: Infectious Diseases Unit, Box 689, University of Rochester School of Medicine, Rochester, NY 14642===</mods:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">État de New York</region></placeName><wicri:cityArea>Correspondence address: Infectious Diseases Unit, Box 689, University of Rochester School of Medicine, Rochester</wicri:cityArea></affiliation></author><author><name sortKey="Nichols, Joan E" sort="Nichols, Joan E" uniqKey="Nichols J" first="Joan E." last="Nichols">Joan E. 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Nichols</name><affiliation wicri:level="2"><mods:affiliation>Infectious Diseases Unit, Department of Medicine, University of Rochester School of Medicine, Rochester, New York</mods:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">État de New York</region></placeName><wicri:cityArea>Infectious Diseases Unit, Department of Medicine, University of Rochester School of Medicine, Rochester</wicri:cityArea></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Journal of Medical Virology</title><title level="j" type="alt">JOURNAL OF MEDICAL VIROLOGY</title><idno type="ISSN">0146-6615</idno><idno type="eISSN">1096-9071</idno><imprint><biblScope unit="vol">27</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="179">179</biblScope><biblScope unit="page" to="187">187</biblScope><biblScope unit="page-count">9</biblScope><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>New York</pubPlace><date type="published" when="1989-03">1989-03</date></imprint><idno type="ISSN">0146-6615</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0146-6615</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Previous studies demonstrated that in vitro infection with influenza A viruses altered several functions of human monocytes‐macrophages but did not detectably alter functions of human lymphocytes. However, both types of cells were infected, as determined by production and surface expression of viral antigens. In the current studies, human mononuclear leukocytes were infected in vitro and assayed for both influenza virus‐induced proliferation and mitogen (phytohemagglutinin [PHA])‐induced proliferation, as well as for ability to stimulate proliferative responses by normal autologous leukocytes. The leukocytes showed proliferation in response to the infectious virus, but concomitant depressed proliferative responses to PHA. Coculture experiments suggested suppression of PHA‐induced responses by the virus‐infected cells. However, upon coculture with fresh autologous leukocytes (without PHA stimulation), both virus‐infected macrophages and virus‐infected lymphocytes induced autologous lymphocyte proliferative responses. Altered proliferative responses to mitogen stimulation after exposure to the virus were not due to diminished interleukin‐1 production or diminished expression of HLA‐DR by monocytes‐macrophages. The expression of influenza virus antigens and resulting induction of autologous proliferative responses, combined with depressed mitogen‐induced proliferation, may be important in human antiviral defense.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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