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Interferon-inducible effector mechanisms in cell-autonomous immunity

Interferons (IFNs) induce the expression of hundreds of genes as part of an elaborate antimicrobial programme designed to combat infection in all nucleated cells — a process termed cell-autonomous immunity. As described in this Review, recent genomic and subgenomic analyses have begun to assign func...

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Autor principal: MacMicking, John D.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4150610/
https://www.ncbi.nlm.nih.gov/pubmed/22531325
http://dx.doi.org/10.1038/nri3210
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author MacMicking, John D.
author_facet MacMicking, John D.
author_sort MacMicking, John D.
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description Interferons (IFNs) induce the expression of hundreds of genes as part of an elaborate antimicrobial programme designed to combat infection in all nucleated cells — a process termed cell-autonomous immunity. As described in this Review, recent genomic and subgenomic analyses have begun to assign functional properties to novel IFN-inducible effector proteins that restrict bacteria, protozoa and viruses in different subcellular compartments and at different stages of the pathogen life cycle. Several newly described host defence factors also participate in canonical oxidative and autophagic pathways by spatially coordinating their activities to enhance microbial killing. Together, these IFN-induced effector networks help to confer vertebrate host resistance to a vast and complex microbial world. SUPPLEMENTARY INFORMATION: The online version of this article (doi:10.1038/nri3210) contains supplementary material, which is available to authorized users.
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spelling pubmed-41506102014-09-01 Interferon-inducible effector mechanisms in cell-autonomous immunity MacMicking, John D. Nat Rev Immunol Article Interferons (IFNs) induce the expression of hundreds of genes as part of an elaborate antimicrobial programme designed to combat infection in all nucleated cells — a process termed cell-autonomous immunity. As described in this Review, recent genomic and subgenomic analyses have begun to assign functional properties to novel IFN-inducible effector proteins that restrict bacteria, protozoa and viruses in different subcellular compartments and at different stages of the pathogen life cycle. Several newly described host defence factors also participate in canonical oxidative and autophagic pathways by spatially coordinating their activities to enhance microbial killing. Together, these IFN-induced effector networks help to confer vertebrate host resistance to a vast and complex microbial world. SUPPLEMENTARY INFORMATION: The online version of this article (doi:10.1038/nri3210) contains supplementary material, which is available to authorized users. Nature Publishing Group UK 2012-04-25 2012 /pmc/articles/PMC4150610/ /pubmed/22531325 http://dx.doi.org/10.1038/nri3210 Text en © Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved. 2012 This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.
spellingShingle Article
MacMicking, John D.
Interferon-inducible effector mechanisms in cell-autonomous immunity
title Interferon-inducible effector mechanisms in cell-autonomous immunity
title_full Interferon-inducible effector mechanisms in cell-autonomous immunity
title_fullStr Interferon-inducible effector mechanisms in cell-autonomous immunity
title_full_unstemmed Interferon-inducible effector mechanisms in cell-autonomous immunity
title_short Interferon-inducible effector mechanisms in cell-autonomous immunity
title_sort interferon-inducible effector mechanisms in cell-autonomous immunity
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4150610/
https://www.ncbi.nlm.nih.gov/pubmed/22531325
http://dx.doi.org/10.1038/nri3210
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