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Type I Interferons as Ambiguous Modulators of Chronic Inflammation in the Central Nervous System

Type I interferons (IFNs) were originally identified as antiviral effector molecules that exert pleiotropic physiological processes ranging from immune modulation, control of proliferation, apoptosis to antitumor activity. However, type I IFNs were recently also shown to apply both beneficial and de...

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Autores principales: Prinz, Marco, Knobeloch, Klaus-Peter
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Research Foundation 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3342377/
https://www.ncbi.nlm.nih.gov/pubmed/22566948
http://dx.doi.org/10.3389/fimmu.2012.00067
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author Prinz, Marco
Knobeloch, Klaus-Peter
author_facet Prinz, Marco
Knobeloch, Klaus-Peter
author_sort Prinz, Marco
collection PubMed
description Type I interferons (IFNs) were originally identified as antiviral effector molecules that exert pleiotropic physiological processes ranging from immune modulation, control of proliferation, apoptosis to antitumor activity. However, type I IFNs were recently also shown to apply both beneficial and detrimental effects to the central nervous system (CNS) and a tightly balanced equilibrium between cellular activation and inhibition seems to be essential to maintain homeostasis within the CNS. In inflammatory pathologies affecting the CNS, type I IFNs are in the center of attention not only because interferon beta (IFN-β) is used as a standard therapeutic in the treatment of relapsing–remitting multiple sclerosis (MS), but also as type I IFN expression is associated with distinct pathologies. Despite the great efficiency of IFN-β in reducing MS relapses and attenuation of novel inflammatory lesions is well documented, underlying molecular mechanisms and cellular target specificities are just beginning to emerge. In contrast to the curative effects, aberrant activation of the type I IFN response were also recently shown to be associated with detrimental effects exemplified by the Aicardi–Goutières syndrome (AGS), a severe disabling autoimmune inflammatory encephalopathy. This review will highlight the dual role of type I interferons during chronic CNS inflammation. Recently uncovered molecular and cellular mechanisms in the etiology of AGS and experimental autoimmune encephalomyelitis (EAE), the murine model of MS will be highlighted.
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spelling pubmed-33423772012-05-07 Type I Interferons as Ambiguous Modulators of Chronic Inflammation in the Central Nervous System Prinz, Marco Knobeloch, Klaus-Peter Front Immunol Immunology Type I interferons (IFNs) were originally identified as antiviral effector molecules that exert pleiotropic physiological processes ranging from immune modulation, control of proliferation, apoptosis to antitumor activity. However, type I IFNs were recently also shown to apply both beneficial and detrimental effects to the central nervous system (CNS) and a tightly balanced equilibrium between cellular activation and inhibition seems to be essential to maintain homeostasis within the CNS. In inflammatory pathologies affecting the CNS, type I IFNs are in the center of attention not only because interferon beta (IFN-β) is used as a standard therapeutic in the treatment of relapsing–remitting multiple sclerosis (MS), but also as type I IFN expression is associated with distinct pathologies. Despite the great efficiency of IFN-β in reducing MS relapses and attenuation of novel inflammatory lesions is well documented, underlying molecular mechanisms and cellular target specificities are just beginning to emerge. In contrast to the curative effects, aberrant activation of the type I IFN response were also recently shown to be associated with detrimental effects exemplified by the Aicardi–Goutières syndrome (AGS), a severe disabling autoimmune inflammatory encephalopathy. This review will highlight the dual role of type I interferons during chronic CNS inflammation. Recently uncovered molecular and cellular mechanisms in the etiology of AGS and experimental autoimmune encephalomyelitis (EAE), the murine model of MS will be highlighted. Frontiers Research Foundation 2012-04-09 /pmc/articles/PMC3342377/ /pubmed/22566948 http://dx.doi.org/10.3389/fimmu.2012.00067 Text en Copyright © 2012 Prinz and Knobeloch. http://www.frontiersin.org/licenseagreement This is an open-access article distributed under the terms of the Creative Commons Attribution Non Commercial License, which permits non-commercial use, distribution, and reproduction in other forums, provided the original authors and source are credited.
spellingShingle Immunology
Prinz, Marco
Knobeloch, Klaus-Peter
Type I Interferons as Ambiguous Modulators of Chronic Inflammation in the Central Nervous System
title Type I Interferons as Ambiguous Modulators of Chronic Inflammation in the Central Nervous System
title_full Type I Interferons as Ambiguous Modulators of Chronic Inflammation in the Central Nervous System
title_fullStr Type I Interferons as Ambiguous Modulators of Chronic Inflammation in the Central Nervous System
title_full_unstemmed Type I Interferons as Ambiguous Modulators of Chronic Inflammation in the Central Nervous System
title_short Type I Interferons as Ambiguous Modulators of Chronic Inflammation in the Central Nervous System
title_sort type i interferons as ambiguous modulators of chronic inflammation in the central nervous system
topic Immunology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3342377/
https://www.ncbi.nlm.nih.gov/pubmed/22566948
http://dx.doi.org/10.3389/fimmu.2012.00067
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