StressCovidV1, Main, Exploration, bibRecord, 000A98

HERP Binds TBK1 To Activate Innate Immunity and Repress Virus Replication in Response to Endoplasmic Reticulum Stress.

Identifieur interne : 000A98 ( Main/Exploration ); précédent : 000A97; suivant : 000A99

HERP Binds TBK1 To Activate Innate Immunity and Repress Virus Replication in Response to Endoplasmic Reticulum Stress.

Source :

Journal of immunology (Baltimore, Md. : 1950) [ 1550-6606 ] ; 2017.

RBID : pubmed:28954889

Descripteurs français

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

Affiliations:

Le document en format XML

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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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<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>
<author><name sortKey="Ge, Maolin" sort="Ge, Maolin" uniqKey="Ge M" first="Maolin" last="Ge">Maolin Ge</name>
<affiliation wicri:level="4"><nlm:affiliation>State Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan 430072, China; and.</nlm:affiliation>
<orgName type="university">Université de Wuhan</orgName>
<country>République populaire de Chine</country>
<placeName><settlement type="city">Wuhan</settlement>
<region type="province">Hubei</region>
</placeName>
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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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<orgName type="university">Université de Wuhan</orgName>
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<region type="province">Hubei</region>
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<author><name sortKey="Cai, Yanyan" sort="Cai, Yanyan" uniqKey="Cai Y" first="Yanyan" last="Cai">Yanyan Cai</name>
<affiliation wicri:level="4"><nlm:affiliation>State Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan 430072, China; and.</nlm:affiliation>
<orgName type="university">Université de Wuhan</orgName>
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<placeName><settlement type="city">Wuhan</settlement>
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</placeName>
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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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<orgName type="university">Université de Wuhan</orgName>
<country>République populaire de Chine</country>
<placeName><settlement type="city">Wuhan</settlement>
<region type="province">Hubei</region>
</placeName>
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</author>
<author><name sortKey="Xiong, Ying" sort="Xiong, Ying" uniqKey="Xiong Y" first="Ying" last="Xiong">Ying Xiong</name>
<affiliation wicri:level="4"><nlm:affiliation>State Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan 430072, China; and.</nlm:affiliation>
<orgName type="university">Université de Wuhan</orgName>
<country>République populaire de Chine</country>
<placeName><settlement type="city">Wuhan</settlement>
<region type="province">Hubei</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Liu, Fang" sort="Liu, Fang" uniqKey="Liu F" first="Fang" last="Liu">Fang Liu</name>
<affiliation wicri:level="4"><nlm:affiliation>State Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan 430072, China; and.</nlm:affiliation>
<orgName type="university">Université de Wuhan</orgName>
<country>République populaire de Chine</country>
<placeName><settlement type="city">Wuhan</settlement>
<region type="province">Hubei</region>
</placeName>
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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>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Interferon Regulatory Factor-3</term>
<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>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<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>
<affiliations><list><country><li>République populaire de Chine</li>
</country>
<region><li>Hubei</li>
</region>
<settlement><li>Wuhan</li>
</settlement>
<orgName><li>Université de Wuhan</li>
</orgName>
</list>
<tree><country name="République populaire de Chine"><region name="Hubei"><name sortKey="Ge, Maolin" sort="Ge, Maolin" uniqKey="Ge M" first="Maolin" last="Ge">Maolin Ge</name>
</region>
<name sortKey="Cai, Yanyan" sort="Cai, Yanyan" uniqKey="Cai Y" first="Yanyan" last="Cai">Yanyan Cai</name>
<name sortKey="Cheng, Xin" sort="Cheng, Xin" uniqKey="Cheng X" first="Xin" last="Cheng">Xin Cheng</name>
<name sortKey="Geng, Qibin" sort="Geng, Qibin" uniqKey="Geng Q" first="Qibin" last="Geng">Qibin Geng</name>
<name sortKey="Liu, Fang" sort="Liu, Fang" uniqKey="Liu F" first="Fang" last="Liu">Fang Liu</name>
<name sortKey="Liu, Yingle" sort="Liu, Yingle" uniqKey="Liu Y" first="Yingle" last="Liu">Yingle Liu</name>
<name sortKey="Luo, Zhen" sort="Luo, Zhen" uniqKey="Luo Z" first="Zhen" last="Luo">Zhen Luo</name>
<name sortKey="Qiao, Zhi" sort="Qiao, Zhi" uniqKey="Qiao Z" first="Zhi" last="Qiao">Zhi Qiao</name>
<name sortKey="Wan, Pin" sort="Wan, Pin" uniqKey="Wan P" first="Pin" last="Wan">Pin Wan</name>
<name sortKey="Wu, Jianguo" sort="Wu, Jianguo" uniqKey="Wu J" first="Jianguo" last="Wu">Jianguo Wu</name>
<name sortKey="Wu, Kailang" sort="Wu, Kailang" uniqKey="Wu K" first="Kailang" last="Wu">Kailang Wu</name>
<name sortKey="Xiong, Ying" sort="Xiong, Ying" uniqKey="Xiong Y" first="Ying" last="Xiong">Ying Xiong</name>
<name sortKey="Zhou, Yao" sort="Zhou, Yao" uniqKey="Zhou Y" first="Yao" last="Zhou">Yao Zhou</name>
</country>
</tree>
</affiliations>
</record>

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HERP Binds TBK1 To Activate Innate Immunity and Repress Virus Replication in Response to Endoplasmic Reticulum Stress.

HERP Binds TBK1 To Activate Innate Immunity and Repress Virus Replication in Response to Endoplasmic Reticulum Stress.

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