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FKBP5 Regulates RIG-I-Mediated NF-κB Activation and Influenza A Virus Infection

Influenza A virus (IAV) is a highly transmissible respiratory pathogen and is a constant threat to global health with considerable economic and social impact. Influenza viral RNA is sensed by host pattern recognition receptors (PRRs), such as the Toll-like receptor 7 (TLR7) and retinoic acid-inducib...

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Autores principales: Hao, Wenzhuo, Wang, Lingyan, Li, Shitao
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7354574/
https://www.ncbi.nlm.nih.gov/pubmed/32580383
http://dx.doi.org/10.3390/v12060672
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author Hao, Wenzhuo
Wang, Lingyan
Li, Shitao
author_facet Hao, Wenzhuo
Wang, Lingyan
Li, Shitao
author_sort Hao, Wenzhuo
collection PubMed
description Influenza A virus (IAV) is a highly transmissible respiratory pathogen and is a constant threat to global health with considerable economic and social impact. Influenza viral RNA is sensed by host pattern recognition receptors (PRRs), such as the Toll-like receptor 7 (TLR7) and retinoic acid-inducible gene I (RIG-I). The activation of these PRRs instigates the interferon regulatory factor (IRF) and nuclear factor kappa B (NF-κB) signaling pathways that induce the expression of interferon-stimulated genes (ISGs) and inflammatory genes. FK506-binding protein 5 (FKBP5) has been implied in the IκBα kinase (IKK) complex. However, the role of FKBP5 in the RIG-I signaling and IAV infection is not well elucidated. Here, we demonstrate that the knockout of FKBP5 increases IAV infection. Furthermore, FKBP5 binds IKKα, which is critical for RIG-I-induced innate immune responses and ISG expression. Taken together, FKBP5 is a novel anti-influenza host factor that restricts IAV infection by the activation of RIG-I-mediated NF-κB signaling.
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spelling pubmed-73545742020-07-23 FKBP5 Regulates RIG-I-Mediated NF-κB Activation and Influenza A Virus Infection Hao, Wenzhuo Wang, Lingyan Li, Shitao Viruses Article Influenza A virus (IAV) is a highly transmissible respiratory pathogen and is a constant threat to global health with considerable economic and social impact. Influenza viral RNA is sensed by host pattern recognition receptors (PRRs), such as the Toll-like receptor 7 (TLR7) and retinoic acid-inducible gene I (RIG-I). The activation of these PRRs instigates the interferon regulatory factor (IRF) and nuclear factor kappa B (NF-κB) signaling pathways that induce the expression of interferon-stimulated genes (ISGs) and inflammatory genes. FK506-binding protein 5 (FKBP5) has been implied in the IκBα kinase (IKK) complex. However, the role of FKBP5 in the RIG-I signaling and IAV infection is not well elucidated. Here, we demonstrate that the knockout of FKBP5 increases IAV infection. Furthermore, FKBP5 binds IKKα, which is critical for RIG-I-induced innate immune responses and ISG expression. Taken together, FKBP5 is a novel anti-influenza host factor that restricts IAV infection by the activation of RIG-I-mediated NF-κB signaling. MDPI 2020-06-22 /pmc/articles/PMC7354574/ /pubmed/32580383 http://dx.doi.org/10.3390/v12060672 Text en © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Hao, Wenzhuo
Wang, Lingyan
Li, Shitao
FKBP5 Regulates RIG-I-Mediated NF-κB Activation and Influenza A Virus Infection
title FKBP5 Regulates RIG-I-Mediated NF-κB Activation and Influenza A Virus Infection
title_full FKBP5 Regulates RIG-I-Mediated NF-κB Activation and Influenza A Virus Infection
title_fullStr FKBP5 Regulates RIG-I-Mediated NF-κB Activation and Influenza A Virus Infection
title_full_unstemmed FKBP5 Regulates RIG-I-Mediated NF-κB Activation and Influenza A Virus Infection
title_short FKBP5 Regulates RIG-I-Mediated NF-κB Activation and Influenza A Virus Infection
title_sort fkbp5 regulates rig-i-mediated nf-κb activation and influenza a virus infection
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7354574/
https://www.ncbi.nlm.nih.gov/pubmed/32580383
http://dx.doi.org/10.3390/v12060672
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