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Response of resting human peripheral blood natural killer cells to interleukin 2

The present study shows that recombinant interleukin 2 (IL-2) purified to homogeneity induces a rapid and potent enhancement of spontaneous cytotoxicity of human peripheral blood lymphocytes. The cells mediating cytotoxicity after 18-h treatment with IL-2 have surface markers of natural killer (NK)...

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Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 1984
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Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2187474/
https://www.ncbi.nlm.nih.gov/pubmed/6434688
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collection PubMed
description The present study shows that recombinant interleukin 2 (IL-2) purified to homogeneity induces a rapid and potent enhancement of spontaneous cytotoxicity of human peripheral blood lymphocytes. The cells mediating cytotoxicity after 18-h treatment with IL-2 have surface markers of natural killer (NK) cells and are generated from the peripheral blood subset containing spontaneous cytotoxic cells. A parallel production of gamma interferon (IFN-gamma) is induced by recombinant IL-2 (rIL-2), and NK cells appear to be the major producer cells, whereas T cells are unable to produce IFN-gamma under these experimental conditions. However, the kinetics of the enhancement of cytotoxicity are faster than those of IFN-gamma production, and monoclonal anti-IFN-gamma antibodies do not suppress this effect, making it unlikely that the IFN- gamma produced is responsible for the enhancement. The enhancement of NK cell activity induced by rIL-2 precedes any proliferative response of the lymphocytes, which is instead observed in longer-term cultures of both NK and T cells.
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spelling pubmed-21874742008-04-17 Response of resting human peripheral blood natural killer cells to interleukin 2 J Exp Med Articles The present study shows that recombinant interleukin 2 (IL-2) purified to homogeneity induces a rapid and potent enhancement of spontaneous cytotoxicity of human peripheral blood lymphocytes. The cells mediating cytotoxicity after 18-h treatment with IL-2 have surface markers of natural killer (NK) cells and are generated from the peripheral blood subset containing spontaneous cytotoxic cells. A parallel production of gamma interferon (IFN-gamma) is induced by recombinant IL-2 (rIL-2), and NK cells appear to be the major producer cells, whereas T cells are unable to produce IFN-gamma under these experimental conditions. However, the kinetics of the enhancement of cytotoxicity are faster than those of IFN-gamma production, and monoclonal anti-IFN-gamma antibodies do not suppress this effect, making it unlikely that the IFN- gamma produced is responsible for the enhancement. The enhancement of NK cell activity induced by rIL-2 precedes any proliferative response of the lymphocytes, which is instead observed in longer-term cultures of both NK and T cells. The Rockefeller University Press 1984-10-01 /pmc/articles/PMC2187474/ /pubmed/6434688 Text en This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).
spellingShingle Articles
Response of resting human peripheral blood natural killer cells to interleukin 2
title Response of resting human peripheral blood natural killer cells to interleukin 2
title_full Response of resting human peripheral blood natural killer cells to interleukin 2
title_fullStr Response of resting human peripheral blood natural killer cells to interleukin 2
title_full_unstemmed Response of resting human peripheral blood natural killer cells to interleukin 2
title_short Response of resting human peripheral blood natural killer cells to interleukin 2
title_sort response of resting human peripheral blood natural killer cells to interleukin 2
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2187474/
https://www.ncbi.nlm.nih.gov/pubmed/6434688