Effect of Influenza A Virus Infection on Natural and Adaptive Cellular Immunity
Identifieur interne : 00C003 ( Main/Merge ); précédent : 00C002; suivant : 00C004Effect of Influenza A Virus Infection on Natural and Adaptive Cellular Immunity
Auteurs : David P. Skoner [États-Unis] ; Theresa L. Whiteside [États-Unis] ; John W. Wilson [États-Unis] ; William J. Doyle [États-Unis] ; Ronald B. Herberman [États-Unis] ; Philip Fireman [États-Unis]Source :
- Clinical Immunology and Immunopathology [ 0090-1229 ] ; 1996.
Descripteurs français
- Wicri :
- topic : Santé publique.
English descriptors
- KwdEn :
- Absolute number, Absolute numbers, Academic press, Allergy clin, Antiviral, Assay, Baseline, Baseline level, Baseline values, Canine kidney cells, Cellular immunity, Class cytotoxic, Clin, Clin influenza virus, Clina, Cryopreserved pbmnc, Current investigation, Current study, Cytotoxic, Different components, Effector cells, Fresh pbmnc, Herberman, Human models, Immune, Immunol, Infection, Innate immunity, Lymphocyte, Lymphocyte subsets, Lytic units, Monoclonal antibodies, Nasal, Nasal lavage, Natural killer, Natural killer cells, Normal response, Nude mice, Pbmnc, Pbmnc proliferation, Pbmnc proliferation assays, Peripheral blood, Pittsburgh cancer institute, Postinoculation days, Proliferation assays, Public health, Same time, Sequential modulation, Skoner, Symptom scores, Terasaki plates, Total lymphocytes, Viral, Viral infections, Virus, Virus antigen, Virus infection, Virus infections, White blood cells.
- Teeft :
- Absolute number, Absolute numbers, Academic press, Allergy clin, Antiviral, Assay, Baseline, Baseline level, Baseline values, Canine kidney cells, Cellular immunity, Class cytotoxic, Clin, Clin influenza virus, Clina, Cryopreserved pbmnc, Current investigation, Current study, Cytotoxic, Different components, Effector cells, Fresh pbmnc, Herberman, Human models, Immune, Immunol, Infection, Innate immunity, Lymphocyte, Lymphocyte subsets, Lytic units, Monoclonal antibodies, Nasal, Nasal lavage, Natural killer, Natural killer cells, Normal response, Nude mice, Pbmnc, Pbmnc proliferation, Pbmnc proliferation assays, Peripheral blood, Pittsburgh cancer institute, Postinoculation days, Proliferation assays, Public health, Same time, Sequential modulation, Skoner, Symptom scores, Terasaki plates, Total lymphocytes, Viral, Viral infections, Virus, Virus antigen, Virus infection, Virus infections, White blood cells.
Abstract
Abstract: Influenza A virus (FLU) is an important pathogen in humans. Although many features of the antiviral immune response have been elucidated in murine and human models of disease, little is known about the role of NK cells, which provide natural, innate immunity. The effects of experimental intranasal FLU (H1N1) inoculation on NK cells and other immune parameters were studied in 18 healthy, adult volunteers during the acute and convalescent phases of infection. Peripheral blood mononuclear cells (PBMNC) were assayed at baseline and on Postinoculation Days 1, 3, 4, 6, 7, 23, and 44. FLU infection and pathophysiologic upper airway responses were documented in all subjects, and there was no mortality. During both the acute (Days 1–3) and the convalescent (Days 23 and 44) stages of the FLU infection, significant increases in NK activity and decreases in the number of activated NK cells were observed. Reductions in the absolute number of T lymphocytes and in PBMNC proliferation to FLU virus antigen and mitogen were also observed. The current investigation extended those findings to include reductions in the number of CD4+and CD8+T lymphocytes and increases in the number of activated T lymphocytes. These results document that FLU infection was accompanied by enhancement of natural immunity and, as expected, suppression of most of the other measured parameters of cellular immunity. The normal response to FLU infection in humans may involve sequential modulation of the different components of the cellular immune system.
Url:
DOI: 10.1006/clin.1996.0082
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<term>Allergy clin</term>
<term>Antiviral</term>
<term>Assay</term>
<term>Baseline</term>
<term>Baseline level</term>
<term>Baseline values</term>
<term>Canine kidney cells</term>
<term>Cellular immunity</term>
<term>Class cytotoxic</term>
<term>Clin</term>
<term>Clin influenza virus</term>
<term>Clina</term>
<term>Cryopreserved pbmnc</term>
<term>Current investigation</term>
<term>Current study</term>
<term>Cytotoxic</term>
<term>Different components</term>
<term>Effector cells</term>
<term>Fresh pbmnc</term>
<term>Herberman</term>
<term>Human models</term>
<term>Immune</term>
<term>Immunol</term>
<term>Infection</term>
<term>Innate immunity</term>
<term>Lymphocyte</term>
<term>Lymphocyte subsets</term>
<term>Lytic units</term>
<term>Monoclonal antibodies</term>
<term>Nasal</term>
<term>Nasal lavage</term>
<term>Natural killer</term>
<term>Natural killer cells</term>
<term>Normal response</term>
<term>Nude mice</term>
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<term>Pbmnc proliferation</term>
<term>Pbmnc proliferation assays</term>
<term>Peripheral blood</term>
<term>Pittsburgh cancer institute</term>
<term>Postinoculation days</term>
<term>Proliferation assays</term>
<term>Public health</term>
<term>Same time</term>
<term>Sequential modulation</term>
<term>Skoner</term>
<term>Symptom scores</term>
<term>Terasaki plates</term>
<term>Total lymphocytes</term>
<term>Viral</term>
<term>Viral infections</term>
<term>Virus</term>
<term>Virus antigen</term>
<term>Virus infection</term>
<term>Virus infections</term>
<term>White blood cells</term>
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<term>Allergy clin</term>
<term>Antiviral</term>
<term>Assay</term>
<term>Baseline</term>
<term>Baseline level</term>
<term>Baseline values</term>
<term>Canine kidney cells</term>
<term>Cellular immunity</term>
<term>Class cytotoxic</term>
<term>Clin</term>
<term>Clin influenza virus</term>
<term>Clina</term>
<term>Cryopreserved pbmnc</term>
<term>Current investigation</term>
<term>Current study</term>
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<term>Different components</term>
<term>Effector cells</term>
<term>Fresh pbmnc</term>
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<term>Human models</term>
<term>Immune</term>
<term>Immunol</term>
<term>Infection</term>
<term>Innate immunity</term>
<term>Lymphocyte</term>
<term>Lymphocyte subsets</term>
<term>Lytic units</term>
<term>Monoclonal antibodies</term>
<term>Nasal</term>
<term>Nasal lavage</term>
<term>Natural killer</term>
<term>Natural killer cells</term>
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<term>Nude mice</term>
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<term>Pbmnc proliferation assays</term>
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<term>Pittsburgh cancer institute</term>
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<term>Proliferation assays</term>
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<term>Sequential modulation</term>
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<term>Symptom scores</term>
<term>Terasaki plates</term>
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<term>Viral infections</term>
<term>Virus</term>
<term>Virus antigen</term>
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<term>Virus infections</term>
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<front><div type="abstract" xml:lang="en">Abstract: Influenza A virus (FLU) is an important pathogen in humans. Although many features of the antiviral immune response have been elucidated in murine and human models of disease, little is known about the role of NK cells, which provide natural, innate immunity. The effects of experimental intranasal FLU (H1N1) inoculation on NK cells and other immune parameters were studied in 18 healthy, adult volunteers during the acute and convalescent phases of infection. Peripheral blood mononuclear cells (PBMNC) were assayed at baseline and on Postinoculation Days 1, 3, 4, 6, 7, 23, and 44. FLU infection and pathophysiologic upper airway responses were documented in all subjects, and there was no mortality. During both the acute (Days 1–3) and the convalescent (Days 23 and 44) stages of the FLU infection, significant increases in NK activity and decreases in the number of activated NK cells were observed. Reductions in the absolute number of T lymphocytes and in PBMNC proliferation to FLU virus antigen and mitogen were also observed. The current investigation extended those findings to include reductions in the number of CD4+and CD8+T lymphocytes and increases in the number of activated T lymphocytes. These results document that FLU infection was accompanied by enhancement of natural immunity and, as expected, suppression of most of the other measured parameters of cellular immunity. The normal response to FLU infection in humans may involve sequential modulation of the different components of the cellular immune system.</div>
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