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Resistance of Natural Killer T Cell–Deficient Mice to Systemic Shwartzman Reaction
The generalized Shwartzman reaction in mice which had been primed and challenged with lipopolysaccharide (LPS) depends on interleukin (IL)-12–induced interferon (IFN)-γ production at the priming stage. We examined the involvement in the priming mechanism of the unique population of Vα14 natural kill...
Autores principales: | , , , , , , , , |
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Formato: | Texto |
Lenguaje: | English |
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The Rockefeller University Press
2000
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2193105/ https://www.ncbi.nlm.nih.gov/pubmed/11104806 |
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author | Dieli, Francesco Sireci, Guido Russo, Domenica Taniguchi, Masaru Ivanyi, Juraj Fernandez, Carmen Troye-Blomberg, Marita De Leo, Giacomo Salerno, Alfredo |
author_facet | Dieli, Francesco Sireci, Guido Russo, Domenica Taniguchi, Masaru Ivanyi, Juraj Fernandez, Carmen Troye-Blomberg, Marita De Leo, Giacomo Salerno, Alfredo |
author_sort | Dieli, Francesco |
collection | PubMed |
description | The generalized Shwartzman reaction in mice which had been primed and challenged with lipopolysaccharide (LPS) depends on interleukin (IL)-12–induced interferon (IFN)-γ production at the priming stage. We examined the involvement in the priming mechanism of the unique population of Vα14 natural killer T (NKT) cells because they promptly produce IFN-γ after IL-12 stimulation. We report here that LPS- or IL-12–primed NKT cell genetically deficient mice were found to be resistant to LPS-elicited mortality. This outcome can be attributed to the reduction of IFN-γ production, because injection of recombinant mouse IFN-γ, but not injection of IL-12, effectively primed the NKT cell–deficient mice. However, priming with high doses of LPS caused mortality of severe combined immunodeficiency, NKT cell–deficient, and CD1-deficient mice, indicating a major contribution of NKT cells to the Shwartzman reaction elicited by low doses of LPS, whereas at higher doses of LPS NK cells play a prominent role. These results suggest that the numerically small NKT cell population of normal mice apparently plays a mandatory role in the priming stage of the generalized Shwartzman reaction. |
format | Text |
id | pubmed-2193105 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2000 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-21931052008-04-16 Resistance of Natural Killer T Cell–Deficient Mice to Systemic Shwartzman Reaction Dieli, Francesco Sireci, Guido Russo, Domenica Taniguchi, Masaru Ivanyi, Juraj Fernandez, Carmen Troye-Blomberg, Marita De Leo, Giacomo Salerno, Alfredo J Exp Med Brief Definitive Report The generalized Shwartzman reaction in mice which had been primed and challenged with lipopolysaccharide (LPS) depends on interleukin (IL)-12–induced interferon (IFN)-γ production at the priming stage. We examined the involvement in the priming mechanism of the unique population of Vα14 natural killer T (NKT) cells because they promptly produce IFN-γ after IL-12 stimulation. We report here that LPS- or IL-12–primed NKT cell genetically deficient mice were found to be resistant to LPS-elicited mortality. This outcome can be attributed to the reduction of IFN-γ production, because injection of recombinant mouse IFN-γ, but not injection of IL-12, effectively primed the NKT cell–deficient mice. However, priming with high doses of LPS caused mortality of severe combined immunodeficiency, NKT cell–deficient, and CD1-deficient mice, indicating a major contribution of NKT cells to the Shwartzman reaction elicited by low doses of LPS, whereas at higher doses of LPS NK cells play a prominent role. These results suggest that the numerically small NKT cell population of normal mice apparently plays a mandatory role in the priming stage of the generalized Shwartzman reaction. The Rockefeller University Press 2000-12-04 /pmc/articles/PMC2193105/ /pubmed/11104806 Text en © 2000 The Rockefeller University Press 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 | Brief Definitive Report Dieli, Francesco Sireci, Guido Russo, Domenica Taniguchi, Masaru Ivanyi, Juraj Fernandez, Carmen Troye-Blomberg, Marita De Leo, Giacomo Salerno, Alfredo Resistance of Natural Killer T Cell–Deficient Mice to Systemic Shwartzman Reaction |
title | Resistance of Natural Killer T Cell–Deficient Mice to Systemic Shwartzman Reaction |
title_full | Resistance of Natural Killer T Cell–Deficient Mice to Systemic Shwartzman Reaction |
title_fullStr | Resistance of Natural Killer T Cell–Deficient Mice to Systemic Shwartzman Reaction |
title_full_unstemmed | Resistance of Natural Killer T Cell–Deficient Mice to Systemic Shwartzman Reaction |
title_short | Resistance of Natural Killer T Cell–Deficient Mice to Systemic Shwartzman Reaction |
title_sort | resistance of natural killer t cell–deficient mice to systemic shwartzman reaction |
topic | Brief Definitive Report |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2193105/ https://www.ncbi.nlm.nih.gov/pubmed/11104806 |
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