Interferon-alpha subtype 11 activates NK cells and enables control of retroviral infection.

The innate immune response mediated by cells such as natural killer (NK) cells is critical for the rapid containment of virus replication and spread during acute infection. Here, we show that subtype 11 of the type I interferon (IFN) family greatly potentiates the antiviral activity of NK cells duri...

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Autores principales:	Kathrin Gibbert, Jara J Joedicke, Andreas Meryk, Mirko Trilling, Sandra Francois, Janine Duppach, Anke Kraft, Karl S Lang, Ulf Dittmer
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2012
Materias:	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/8a9c4e555e654d089ea8c3a31ce2cd58
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spelling	oai:doaj.org-article:8a9c4e555e654d089ea8c3a31ce2cd582021-11-18T06:04:05ZInterferon-alpha subtype 11 activates NK cells and enables control of retroviral infection.1553-73661553-737410.1371/journal.ppat.1002868https://doaj.org/article/8a9c4e555e654d089ea8c3a31ce2cd582012-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22912583/pdf/?tool=EBIhttps://doaj.org/toc/1553-7366https://doaj.org/toc/1553-7374The innate immune response mediated by cells such as natural killer (NK) cells is critical for the rapid containment of virus replication and spread during acute infection. Here, we show that subtype 11 of the type I interferon (IFN) family greatly potentiates the antiviral activity of NK cells during retroviral infection. Treatment of mice with IFN-α11 during Friend retrovirus infection (FV) significantly reduced viral loads and resulted in long-term protection from virus-induced leukemia. The effect of IFN-α11 on NK cells was direct and signaled through the type I IFN receptor. Furthermore, IFN-α11-mediated activation of NK cells enabled cytolytic killing of FV-infected target cells via the exocytosis pathway. Depletion and adoptive transfer experiments illustrated that NK cells played a major role in successful IFN-α11 therapy. Additional experiments with Mouse Cytomegalovirus infections demonstrated that the therapeutic effect of IFN-α11 is not restricted to retroviruses. The type I IFN subtypes 2 and 5, which bind the same receptor as IFN-α11, did not elicit similar antiviral effects. These results demonstrate a unique and subtype-specific activation of NK cells by IFN-α11.Kathrin GibbertJara J JoedickeAndreas MerykMirko TrillingSandra FrancoisJanine DuppachAnke KraftKarl S LangUlf DittmerPublic Library of Science (PLoS)articleImmunologic diseases. AllergyRC581-607Biology (General)QH301-705.5ENPLoS Pathogens, Vol 8, Iss 8, p e1002868 (2012)
institution	DOAJ
collection	DOAJ
language	EN
topic	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5
spellingShingle	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5 Kathrin Gibbert Jara J Joedicke Andreas Meryk Mirko Trilling Sandra Francois Janine Duppach Anke Kraft Karl S Lang Ulf Dittmer Interferon-alpha subtype 11 activates NK cells and enables control of retroviral infection.
description	The innate immune response mediated by cells such as natural killer (NK) cells is critical for the rapid containment of virus replication and spread during acute infection. Here, we show that subtype 11 of the type I interferon (IFN) family greatly potentiates the antiviral activity of NK cells during retroviral infection. Treatment of mice with IFN-α11 during Friend retrovirus infection (FV) significantly reduced viral loads and resulted in long-term protection from virus-induced leukemia. The effect of IFN-α11 on NK cells was direct and signaled through the type I IFN receptor. Furthermore, IFN-α11-mediated activation of NK cells enabled cytolytic killing of FV-infected target cells via the exocytosis pathway. Depletion and adoptive transfer experiments illustrated that NK cells played a major role in successful IFN-α11 therapy. Additional experiments with Mouse Cytomegalovirus infections demonstrated that the therapeutic effect of IFN-α11 is not restricted to retroviruses. The type I IFN subtypes 2 and 5, which bind the same receptor as IFN-α11, did not elicit similar antiviral effects. These results demonstrate a unique and subtype-specific activation of NK cells by IFN-α11.
format	article
author	Kathrin Gibbert Jara J Joedicke Andreas Meryk Mirko Trilling Sandra Francois Janine Duppach Anke Kraft Karl S Lang Ulf Dittmer
author_facet	Kathrin Gibbert Jara J Joedicke Andreas Meryk Mirko Trilling Sandra Francois Janine Duppach Anke Kraft Karl S Lang Ulf Dittmer
author_sort	Kathrin Gibbert
title	Interferon-alpha subtype 11 activates NK cells and enables control of retroviral infection.
title_short	Interferon-alpha subtype 11 activates NK cells and enables control of retroviral infection.
title_full	Interferon-alpha subtype 11 activates NK cells and enables control of retroviral infection.
title_fullStr	Interferon-alpha subtype 11 activates NK cells and enables control of retroviral infection.
title_full_unstemmed	Interferon-alpha subtype 11 activates NK cells and enables control of retroviral infection.
title_sort	interferon-alpha subtype 11 activates nk cells and enables control of retroviral infection.
publisher	Public Library of Science (PLoS)
publishDate	2012
url	https://doaj.org/article/8a9c4e555e654d089ea8c3a31ce2cd58
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Interferon-alpha subtype 11 activates NK cells and enables control of retroviral infection.

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