HERP Binds TBK1 To Activate Innate Immunity and Repress Virus Replication in Response to Endoplasmic Reticulum Stress.
Identifieur interne : 000A98 ( Main/Curation ); précédent : 000A97; suivant : 000A99HERP Binds TBK1 To Activate Innate Immunity and Repress Virus Replication in Response to Endoplasmic Reticulum Stress.
Auteurs : Maolin Ge [République populaire de Chine] ; Zhen Luo [République populaire de Chine] ; Zhi Qiao [République populaire de Chine] ; Yao Zhou [République populaire de Chine] ; Xin Cheng [République populaire de Chine] ; Qibin Geng [République populaire de Chine] ; Yanyan Cai [République populaire de Chine] ; Pin Wan [République populaire de Chine] ; Ying Xiong [République populaire de Chine] ; Fang Liu [République populaire de Chine] ; Kailang Wu [République populaire de Chine] ; Yingle Liu [République populaire de Chine] ; Jianguo Wu [République populaire de Chine]Source :
- Journal of immunology (Baltimore, Md. : 1950) [ 1550-6606 ] ; 2017.
Descripteurs français
- KwdFr :
- Animaux, Facteur-3 de régulation d'interféron (génétique), Facteur-3 de régulation d'interféron (immunologie), Femelle, Humains, Immunité innée, Infections à virus à ARN (anatomopathologie), Infections à virus à ARN (génétique), Infections à virus à ARN (immunologie), Interférons (génétique), Interférons (immunologie), Mâle, Protein-Serine-Threonine Kinases (génétique), Protein-Serine-Threonine Kinases (immunologie), Protéines membranaires (génétique), Protéines membranaires (immunologie), Réplication virale (immunologie), Souris, Souris de lignée BALB C, Stress du réticulum endoplasmique (génétique), Stress du réticulum endoplasmique (immunologie), Virus à ARN (physiologie).
- MESH :
- anatomopathologie : Infections à virus à ARN.
- génétique : Facteur-3 de régulation d'interféron, Infections à virus à ARN, Interférons, Protein-Serine-Threonine Kinases, Protéines membranaires, Stress du réticulum endoplasmique.
- immunologie : Facteur-3 de régulation d'interféron, Infections à virus à ARN, Interférons, Protein-Serine-Threonine Kinases, Protéines membranaires, Réplication virale, Stress du réticulum endoplasmique.
- physiologie : Virus à ARN.
- Animaux, Femelle, Humains, Immunité innée, Mâle, Souris, Souris de lignée BALB C.
English descriptors
- KwdEn :
- Animals, Endoplasmic Reticulum Stress (genetics), Endoplasmic Reticulum Stress (immunology), Female, Humans, Immunity, Innate, Interferon Regulatory Factor-3 (genetics), Interferon Regulatory Factor-3 (immunology), Interferons (genetics), Interferons (immunology), Male, Membrane Proteins (genetics), Membrane Proteins (immunology), Mice, Mice, Inbred BALB C, Protein-Serine-Threonine Kinases (genetics), Protein-Serine-Threonine Kinases (immunology), RNA Virus Infections (genetics), RNA Virus Infections (immunology), RNA Virus Infections (pathology), RNA Viruses (physiology), Virus Replication (immunology).
- MESH :
- chemical , genetics : Interferon Regulatory Factor-3, Interferons, Membrane Proteins, Protein-Serine-Threonine Kinases.
- genetics : Endoplasmic Reticulum Stress, RNA Virus Infections.
- immunology : Endoplasmic Reticulum Stress, Interferon Regulatory Factor-3, Interferons, Membrane Proteins, Protein-Serine-Threonine Kinases, RNA Virus Infections, Virus Replication.
- pathology : RNA Virus Infections.
- physiology : RNA Viruses.
- Animals, Female, Humans, Immunity, Innate, Male, Mice, Mice, Inbred BALB C.
Abstract
Host innate immunity is crucial for cellular responses against viral infection sensed by distinct pattern recognition receptors and endoplasmic reticulum (ER) stress. Enterovirus 71 (EV71) is a causative agent of hand, foot, and mouth disease and neurological diseases. However, the exact mechanism underlying the link between ER stress induced by EV71 infection and host innate immunity is largely unknown. In this study, we demonstrated that EV71 infection induces the homocysteine-induced ER protein (HERP), a modulator of the ER stress response which is dependent on the participation of MAVS. Virus-induced HERP subsequently stimulates host innate immunity to repress viral replication by promoting type-I IFNs (IFN-α and IFN-β) and type-III IFN (IFN-λ1) expression. Through interacting with TANK-binding kinase 1, HERP amplifies the MAVS signaling and facilitates the phosphorylation and nuclear translocation of IFN regulatory factor 3 and NF-κB to enhance the expression of IFNs, which leads to a broad inhibition of the replication of RNA viruses, including EV71, Sendai virus, influenza A virus, and vesicular stomatitis virus. Therefore, we demonstrated that HERP plays an important role in the regulation of host innate immunity in response to ER stress during the infection of RNA viruses. These findings provide new insights into the mechanism underlying the replication of RNA viruses and the production of IFNs, and also demonstrate a new role of HERP in the regulation of host innate immunity in response to viral infection.
DOI: 10.4049/jimmunol.1700376
PubMed: 28954889
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pubmed:28954889Le document en format XML
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<sourceDesc><biblStruct><analytic><title xml:lang="en">HERP Binds TBK1 To Activate Innate Immunity and Repress Virus Replication in Response to Endoplasmic Reticulum Stress.</title>
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<author><name sortKey="Luo, Zhen" sort="Luo, Zhen" uniqKey="Luo Z" first="Zhen" last="Luo">Zhen Luo</name>
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<author><name sortKey="Qiao, Zhi" sort="Qiao, Zhi" uniqKey="Qiao Z" first="Zhi" last="Qiao">Zhi Qiao</name>
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<author><name sortKey="Cai, Yanyan" sort="Cai, Yanyan" uniqKey="Cai Y" first="Yanyan" last="Cai">Yanyan Cai</name>
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<author><name sortKey="Wan, Pin" sort="Wan, Pin" uniqKey="Wan P" first="Pin" last="Wan">Pin Wan</name>
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<author><name sortKey="Xiong, Ying" sort="Xiong, Ying" uniqKey="Xiong Y" first="Ying" last="Xiong">Ying Xiong</name>
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<author><name sortKey="Liu, Fang" sort="Liu, Fang" uniqKey="Liu F" first="Fang" last="Liu">Fang Liu</name>
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<author><name sortKey="Wu, Kailang" sort="Wu, Kailang" uniqKey="Wu K" first="Kailang" last="Wu">Kailang Wu</name>
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<author><name sortKey="Liu, Yingle" sort="Liu, Yingle" uniqKey="Liu Y" first="Yingle" last="Liu">Yingle Liu</name>
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<author><name sortKey="Wu, Jianguo" sort="Wu, Jianguo" uniqKey="Wu J" first="Jianguo" last="Wu">Jianguo Wu</name>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term>
<term>Endoplasmic Reticulum Stress (genetics)</term>
<term>Endoplasmic Reticulum Stress (immunology)</term>
<term>Female</term>
<term>Humans</term>
<term>Immunity, Innate</term>
<term>Interferon Regulatory Factor-3 (genetics)</term>
<term>Interferon Regulatory Factor-3 (immunology)</term>
<term>Interferons (genetics)</term>
<term>Interferons (immunology)</term>
<term>Male</term>
<term>Membrane Proteins (genetics)</term>
<term>Membrane Proteins (immunology)</term>
<term>Mice</term>
<term>Mice, Inbred BALB C</term>
<term>Protein-Serine-Threonine Kinases (genetics)</term>
<term>Protein-Serine-Threonine Kinases (immunology)</term>
<term>RNA Virus Infections (genetics)</term>
<term>RNA Virus Infections (immunology)</term>
<term>RNA Virus Infections (pathology)</term>
<term>RNA Viruses (physiology)</term>
<term>Virus Replication (immunology)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term>
<term>Facteur-3 de régulation d'interféron (génétique)</term>
<term>Facteur-3 de régulation d'interféron (immunologie)</term>
<term>Femelle</term>
<term>Humains</term>
<term>Immunité innée</term>
<term>Infections à virus à ARN (anatomopathologie)</term>
<term>Infections à virus à ARN (génétique)</term>
<term>Infections à virus à ARN (immunologie)</term>
<term>Interférons (génétique)</term>
<term>Interférons (immunologie)</term>
<term>Mâle</term>
<term>Protein-Serine-Threonine Kinases (génétique)</term>
<term>Protein-Serine-Threonine Kinases (immunologie)</term>
<term>Protéines membranaires (génétique)</term>
<term>Protéines membranaires (immunologie)</term>
<term>Réplication virale (immunologie)</term>
<term>Souris</term>
<term>Souris de lignée BALB C</term>
<term>Stress du réticulum endoplasmique (génétique)</term>
<term>Stress du réticulum endoplasmique (immunologie)</term>
<term>Virus à ARN (physiologie)</term>
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<term>Interferons</term>
<term>Membrane Proteins</term>
<term>Protein-Serine-Threonine Kinases</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Infections à virus à ARN</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Endoplasmic Reticulum Stress</term>
<term>RNA Virus Infections</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Facteur-3 de régulation d'interféron</term>
<term>Infections à virus à ARN</term>
<term>Interférons</term>
<term>Protein-Serine-Threonine Kinases</term>
<term>Protéines membranaires</term>
<term>Stress du réticulum endoplasmique</term>
</keywords>
<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Facteur-3 de régulation d'interféron</term>
<term>Infections à virus à ARN</term>
<term>Interférons</term>
<term>Protein-Serine-Threonine Kinases</term>
<term>Protéines membranaires</term>
<term>Réplication virale</term>
<term>Stress du réticulum endoplasmique</term>
</keywords>
<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Endoplasmic Reticulum Stress</term>
<term>Interferon Regulatory Factor-3</term>
<term>Interferons</term>
<term>Membrane Proteins</term>
<term>Protein-Serine-Threonine Kinases</term>
<term>RNA Virus Infections</term>
<term>Virus Replication</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>RNA Virus Infections</term>
</keywords>
<keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Virus à ARN</term>
</keywords>
<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>RNA Viruses</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Female</term>
<term>Humans</term>
<term>Immunity, Innate</term>
<term>Male</term>
<term>Mice</term>
<term>Mice, Inbred BALB C</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Femelle</term>
<term>Humains</term>
<term>Immunité innée</term>
<term>Mâle</term>
<term>Souris</term>
<term>Souris de lignée BALB C</term>
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<front><div type="abstract" xml:lang="en">Host innate immunity is crucial for cellular responses against viral infection sensed by distinct pattern recognition receptors and endoplasmic reticulum (ER) stress. Enterovirus 71 (EV71) is a causative agent of hand, foot, and mouth disease and neurological diseases. However, the exact mechanism underlying the link between ER stress induced by EV71 infection and host innate immunity is largely unknown. In this study, we demonstrated that EV71 infection induces the homocysteine-induced ER protein (HERP), a modulator of the ER stress response which is dependent on the participation of MAVS. Virus-induced HERP subsequently stimulates host innate immunity to repress viral replication by promoting type-I IFNs (IFN-α and IFN-β) and type-III IFN (IFN-λ1) expression. Through interacting with TANK-binding kinase 1, HERP amplifies the MAVS signaling and facilitates the phosphorylation and nuclear translocation of IFN regulatory factor 3 and NF-κB to enhance the expression of IFNs, which leads to a broad inhibition of the replication of RNA viruses, including EV71, Sendai virus, influenza A virus, and vesicular stomatitis virus. Therefore, we demonstrated that HERP plays an important role in the regulation of host innate immunity in response to ER stress during the infection of RNA viruses. These findings provide new insights into the mechanism underlying the replication of RNA viruses and the production of IFNs, and also demonstrate a new role of HERP in the regulation of host innate immunity in response to viral infection.</div>
</front>
</TEI>
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