IL-33 contributes to sepsis-induced long-term immunosuppression by expanding the regulatory T cell population

Patients who survive sepsis are at increased risk of infection owing to long-term immunosuppression that is associated with an increase in Treg cell numbers. Here the authors show expansion of the Treg cell population in sepsis mice is driven by IL-33-induced ILC2 activation of IL-10 production by m...

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Autores principales: Daniele C. Nascimento, Paulo H. Melo, Annie R. Piñeros, Raphael G. Ferreira, David F. Colón, Paula B. Donate, Fernanda V. Castanheira, Aline Gozzi, Paula G. Czaikoski, Wanda Niedbala, Marcos C. Borges, Dario S. Zamboni, Foo Y. Liew, Fernando Q. Cunha, Jose C. Alves-Filho
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Publicado: Nature Portfolio 2017
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Acceso en línea:https://doaj.org/article/14c052279c2943bbbeef427db07d64ab
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spelling oai:doaj.org-article:14c052279c2943bbbeef427db07d64ab2021-12-02T14:42:42ZIL-33 contributes to sepsis-induced long-term immunosuppression by expanding the regulatory T cell population10.1038/ncomms149192041-1723https://doaj.org/article/14c052279c2943bbbeef427db07d64ab2017-04-01T00:00:00Zhttps://doi.org/10.1038/ncomms14919https://doaj.org/toc/2041-1723Patients who survive sepsis are at increased risk of infection owing to long-term immunosuppression that is associated with an increase in Treg cell numbers. Here the authors show expansion of the Treg cell population in sepsis mice is driven by IL-33-induced ILC2 activation of IL-10 production by macrophages.Daniele C. NascimentoPaulo H. MeloAnnie R. PiñerosRaphael G. FerreiraDavid F. ColónPaula B. DonateFernanda V. CastanheiraAline GozziPaula G. CzaikoskiWanda NiedbalaMarcos C. BorgesDario S. ZamboniFoo Y. LiewFernando Q. CunhaJose C. Alves-FilhoNature PortfolioarticleScienceQENNature Communications, Vol 8, Iss 1, Pp 1-14 (2017)
institution DOAJ
collection DOAJ
language EN
topic Science
Q
spellingShingle Science
Q
Daniele C. Nascimento
Paulo H. Melo
Annie R. Piñeros
Raphael G. Ferreira
David F. Colón
Paula B. Donate
Fernanda V. Castanheira
Aline Gozzi
Paula G. Czaikoski
Wanda Niedbala
Marcos C. Borges
Dario S. Zamboni
Foo Y. Liew
Fernando Q. Cunha
Jose C. Alves-Filho
IL-33 contributes to sepsis-induced long-term immunosuppression by expanding the regulatory T cell population
description Patients who survive sepsis are at increased risk of infection owing to long-term immunosuppression that is associated with an increase in Treg cell numbers. Here the authors show expansion of the Treg cell population in sepsis mice is driven by IL-33-induced ILC2 activation of IL-10 production by macrophages.
format article
author Daniele C. Nascimento
Paulo H. Melo
Annie R. Piñeros
Raphael G. Ferreira
David F. Colón
Paula B. Donate
Fernanda V. Castanheira
Aline Gozzi
Paula G. Czaikoski
Wanda Niedbala
Marcos C. Borges
Dario S. Zamboni
Foo Y. Liew
Fernando Q. Cunha
Jose C. Alves-Filho
author_facet Daniele C. Nascimento
Paulo H. Melo
Annie R. Piñeros
Raphael G. Ferreira
David F. Colón
Paula B. Donate
Fernanda V. Castanheira
Aline Gozzi
Paula G. Czaikoski
Wanda Niedbala
Marcos C. Borges
Dario S. Zamboni
Foo Y. Liew
Fernando Q. Cunha
Jose C. Alves-Filho
author_sort Daniele C. Nascimento
title IL-33 contributes to sepsis-induced long-term immunosuppression by expanding the regulatory T cell population
title_short IL-33 contributes to sepsis-induced long-term immunosuppression by expanding the regulatory T cell population
title_full IL-33 contributes to sepsis-induced long-term immunosuppression by expanding the regulatory T cell population
title_fullStr IL-33 contributes to sepsis-induced long-term immunosuppression by expanding the regulatory T cell population
title_full_unstemmed IL-33 contributes to sepsis-induced long-term immunosuppression by expanding the regulatory T cell population
title_sort il-33 contributes to sepsis-induced long-term immunosuppression by expanding the regulatory t cell population
publisher Nature Portfolio
publishDate 2017
url https://doaj.org/article/14c052279c2943bbbeef427db07d64ab
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