IL-33 induction and signaling are controlled by glutaredoxin-1 in mouse macrophages.
Identifieur interne : 000156 ( Main/Exploration ); précédent : 000155; suivant : 000157IL-33 induction and signaling are controlled by glutaredoxin-1 in mouse macrophages.
Auteurs : Ellen O. Weinberg [États-Unis] ; Beatriz Ferran [États-Unis] ; Yuko Tsukahara [États-Unis] ; Michaela M S. Hatch [États-Unis] ; Jingyan Han [États-Unis] ; Colin E. Murdoch [États-Unis] ; Reiko Matsui [États-Unis]Source :
- PloS one [ 1932-6203 ] ; 2019.
Descripteurs français
- KwdFr :
- ARN messager (génétique), ARN messager (métabolisme), Allergènes (administration et posologie), Animaux (MeSH), Asthme (immunologie), Asthme (métabolisme), Asthme (étiologie), Cellules RAW 264.7 (MeSH), Expression des gènes (effets des médicaments et des substances chimiques), Facteur de transcription NF-kappa B (métabolisme), Facteur-6 associé aux récepteurs de TNF (métabolisme), Glutarédoxines (déficit), Glutarédoxines (génétique), Glutarédoxines (métabolisme), Glutathion (métabolisme), Interleukine-33 (biosynthèse), Interleukine-33 (génétique), Lipopolysaccharides (pharmacologie), Macrophages (effets des médicaments et des substances chimiques), Macrophages (immunologie), Macrophages (métabolisme), Modèles animaux de maladie humaine (MeSH), Petit ARN interférent (génétique), Poumon (immunologie), Poumon (métabolisme), Souris (MeSH), Souris knockout (MeSH), Techniques de knock-down de gènes (MeSH), Transduction du signal (MeSH).
- MESH :
- administration et posologie : Allergènes.
- biosynthèse : Interleukine-33.
- déficit : Glutarédoxines.
- effets des médicaments et des substances chimiques : Expression des gènes, Macrophages.
- génétique : ARN messager, Glutarédoxines, Interleukine-33, Petit ARN interférent.
- immunologie : Asthme, Macrophages, Poumon.
- métabolisme : ARN messager, Asthme, Facteur de transcription NF-kappa B, Facteur-6 associé aux récepteurs de TNF, Glutarédoxines, Glutathion, Macrophages, Poumon.
- pharmacologie : Lipopolysaccharides.
- étiologie : Asthme.
- Animaux, Cellules RAW 264.7, Modèles animaux de maladie humaine, Souris, Souris knockout, Techniques de knock-down de gènes, Transduction du signal.
English descriptors
- KwdEn :
- Allergens (administration & dosage), Animals (MeSH), Asthma (etiology), Asthma (immunology), Asthma (metabolism), Disease Models, Animal (MeSH), Gene Expression (drug effects), Gene Knockdown Techniques (MeSH), Glutaredoxins (deficiency), Glutaredoxins (genetics), Glutaredoxins (metabolism), Glutathione (metabolism), Interleukin-33 (biosynthesis), Interleukin-33 (genetics), Lipopolysaccharides (pharmacology), Lung (immunology), Lung (metabolism), Macrophages (drug effects), Macrophages (immunology), Macrophages (metabolism), Mice (MeSH), Mice, Knockout (MeSH), NF-kappa B (metabolism), RAW 264.7 Cells (MeSH), RNA, Messenger (genetics), RNA, Messenger (metabolism), RNA, Small Interfering (genetics), Signal Transduction (MeSH), TNF Receptor-Associated Factor 6 (metabolism).
- MESH :
- chemical , administration & dosage : Allergens.
- chemical , biosynthesis : Interleukin-33.
- chemical , deficiency : Glutaredoxins.
- drug effects : Gene Expression, Macrophages.
- etiology : Asthma.
- chemical , genetics : Glutaredoxins, Interleukin-33, RNA, Messenger, RNA, Small Interfering.
- immunology : Asthma, Lung, Macrophages.
- metabolism : Asthma, Glutaredoxins, Glutathione, Lung, Macrophages, NF-kappa B, RNA, Messenger, TNF Receptor-Associated Factor 6.
- chemical , pharmacology : Lipopolysaccharides.
- Animals, Disease Models, Animal, Gene Knockdown Techniques, Mice, Mice, Knockout, RAW 264.7 Cells, Signal Transduction.
Abstract
Interleukin (IL)-33 is an interleukin-1 like cytokine that enhances Th2 responses and mediates mucosal immunity and allergic inflammation but the mechanism regulating endogenous IL-33 production are still under investigation. In macrophages, lipopolysaccharide (LPS) administration resulted in marked induction of IL-33 mRNA that was blunted in macrophages from glutaredoxin-1 (Glrx) knockout mice and in RAW264.7 macrophages with Glrx knockdown by siRNA. Glutaredoxin-1 is a small cytosolic thioltransferase that controls a reversible protein thiol modification, S-glutationylation (protein-GSH adducts), thereby regulating redox signaling. In this study, we examined the mechanism of Glrx regulation of endogenous IL-33 induction in macrophages. Glrx knockdown resulted in impaired de-glutathionylation of TRAF6, which is required for TRAF6 activation, and inhibited downstream IKKβ and NF-κB activation. Inhibitors of NF-κB suppressed IL-33 induction and chromatin IP sequencing data analysis confirmed that IL-33 is an NF-κB-responsive gene. Since TRAF6-NF-κB activation is also essential for IL-33 signaling through its receptor, ST2L, we next tested the involvement of Glrx in exogenous IL-33 responses in RAW264.7 cells. Recombinant IL-33 (rIL-33) administration induced IL-33 mRNA expression in RAW264.7 macrophages, and this was inhibited by Glrx knockdown. Interestingly, rIL-33-induced IL-33 protein was identified as the 20 kDa cleaved form whereas LPS-induced IL-33 protein was identified as full-length IL-33, which may be less active than the cleaved form. In a clinically-relevant mouse model of asthma, intra-tracheal cockroach antigen treatment induced Glrx protein in wild type mouse lungs but Glrx induction was attenuated in IL-33 knockout mouse lungs, suggesting that IL-33 may regulate Glrx induction in vivo in response to allergen challenge. In summary, our data reveal a novel mechanism by which Glrx controls both LPS- and IL-33-mediated NF-κB activation leading to IL-33 production, and paracrine IL-33 can induce Glrx to further regulate inflammatory reactions.
DOI: 10.1371/journal.pone.0210827
PubMed: 30682073
PubMed Central: PMC6347181
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">IL-33 induction and signaling are controlled by glutaredoxin-1 in mouse macrophages.</title>
<author><name sortKey="Weinberg, Ellen O" sort="Weinberg, Ellen O" uniqKey="Weinberg E" first="Ellen O" last="Weinberg">Ellen O. Weinberg</name>
<affiliation wicri:level="2"><nlm:affiliation>Department of Medicine, Section of Infectious Diseases, Boston University School of Medicine, Boston, Massachusetts, United States of America.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Medicine, Section of Infectious Diseases, Boston University School of Medicine, Boston, Massachusetts</wicri:regionArea>
<placeName><region type="state">Massachusetts</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Ferran, Beatriz" sort="Ferran, Beatriz" uniqKey="Ferran B" first="Beatriz" last="Ferran">Beatriz Ferran</name>
<affiliation wicri:level="2"><nlm:affiliation>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, United States of America.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts</wicri:regionArea>
<placeName><region type="state">Massachusetts</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Tsukahara, Yuko" sort="Tsukahara, Yuko" uniqKey="Tsukahara Y" first="Yuko" last="Tsukahara">Yuko Tsukahara</name>
<affiliation wicri:level="2"><nlm:affiliation>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, United States of America.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts</wicri:regionArea>
<placeName><region type="state">Massachusetts</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Hatch, Michaela M S" sort="Hatch, Michaela M S" uniqKey="Hatch M" first="Michaela M S" last="Hatch">Michaela M S. Hatch</name>
<affiliation wicri:level="2"><nlm:affiliation>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, United States of America.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts</wicri:regionArea>
<placeName><region type="state">Massachusetts</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Han, Jingyan" sort="Han, Jingyan" uniqKey="Han J" first="Jingyan" last="Han">Jingyan Han</name>
<affiliation wicri:level="2"><nlm:affiliation>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, United States of America.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts</wicri:regionArea>
<placeName><region type="state">Massachusetts</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Murdoch, Colin E" sort="Murdoch, Colin E" uniqKey="Murdoch C" first="Colin E" last="Murdoch">Colin E. Murdoch</name>
<affiliation wicri:level="2"><nlm:affiliation>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, United States of America.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts</wicri:regionArea>
<placeName><region type="state">Massachusetts</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Matsui, Reiko" sort="Matsui, Reiko" uniqKey="Matsui R" first="Reiko" last="Matsui">Reiko Matsui</name>
<affiliation wicri:level="2"><nlm:affiliation>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, United States of America.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts</wicri:regionArea>
<placeName><region type="state">Massachusetts</region>
</placeName>
</affiliation>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">PubMed</idno>
<date when="2019">2019</date>
<idno type="RBID">pubmed:30682073</idno>
<idno type="pmid">30682073</idno>
<idno type="doi">10.1371/journal.pone.0210827</idno>
<idno type="pmc">PMC6347181</idno>
<idno type="wicri:Area/Main/Corpus">000167</idno>
<idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000167</idno>
<idno type="wicri:Area/Main/Curation">000167</idno>
<idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Curation">000167</idno>
<idno type="wicri:Area/Main/Exploration">000167</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title xml:lang="en">IL-33 induction and signaling are controlled by glutaredoxin-1 in mouse macrophages.</title>
<author><name sortKey="Weinberg, Ellen O" sort="Weinberg, Ellen O" uniqKey="Weinberg E" first="Ellen O" last="Weinberg">Ellen O. Weinberg</name>
<affiliation wicri:level="2"><nlm:affiliation>Department of Medicine, Section of Infectious Diseases, Boston University School of Medicine, Boston, Massachusetts, United States of America.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Medicine, Section of Infectious Diseases, Boston University School of Medicine, Boston, Massachusetts</wicri:regionArea>
<placeName><region type="state">Massachusetts</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Ferran, Beatriz" sort="Ferran, Beatriz" uniqKey="Ferran B" first="Beatriz" last="Ferran">Beatriz Ferran</name>
<affiliation wicri:level="2"><nlm:affiliation>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, United States of America.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts</wicri:regionArea>
<placeName><region type="state">Massachusetts</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Tsukahara, Yuko" sort="Tsukahara, Yuko" uniqKey="Tsukahara Y" first="Yuko" last="Tsukahara">Yuko Tsukahara</name>
<affiliation wicri:level="2"><nlm:affiliation>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, United States of America.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts</wicri:regionArea>
<placeName><region type="state">Massachusetts</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Hatch, Michaela M S" sort="Hatch, Michaela M S" uniqKey="Hatch M" first="Michaela M S" last="Hatch">Michaela M S. Hatch</name>
<affiliation wicri:level="2"><nlm:affiliation>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, United States of America.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts</wicri:regionArea>
<placeName><region type="state">Massachusetts</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Han, Jingyan" sort="Han, Jingyan" uniqKey="Han J" first="Jingyan" last="Han">Jingyan Han</name>
<affiliation wicri:level="2"><nlm:affiliation>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, United States of America.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts</wicri:regionArea>
<placeName><region type="state">Massachusetts</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Murdoch, Colin E" sort="Murdoch, Colin E" uniqKey="Murdoch C" first="Colin E" last="Murdoch">Colin E. Murdoch</name>
<affiliation wicri:level="2"><nlm:affiliation>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, United States of America.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts</wicri:regionArea>
<placeName><region type="state">Massachusetts</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Matsui, Reiko" sort="Matsui, Reiko" uniqKey="Matsui R" first="Reiko" last="Matsui">Reiko Matsui</name>
<affiliation wicri:level="2"><nlm:affiliation>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, United States of America.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts</wicri:regionArea>
<placeName><region type="state">Massachusetts</region>
</placeName>
</affiliation>
</author>
</analytic>
<series><title level="j">PloS one</title>
<idno type="eISSN">1932-6203</idno>
<imprint><date when="2019" type="published">2019</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Allergens (administration & dosage)</term>
<term>Animals (MeSH)</term>
<term>Asthma (etiology)</term>
<term>Asthma (immunology)</term>
<term>Asthma (metabolism)</term>
<term>Disease Models, Animal (MeSH)</term>
<term>Gene Expression (drug effects)</term>
<term>Gene Knockdown Techniques (MeSH)</term>
<term>Glutaredoxins (deficiency)</term>
<term>Glutaredoxins (genetics)</term>
<term>Glutaredoxins (metabolism)</term>
<term>Glutathione (metabolism)</term>
<term>Interleukin-33 (biosynthesis)</term>
<term>Interleukin-33 (genetics)</term>
<term>Lipopolysaccharides (pharmacology)</term>
<term>Lung (immunology)</term>
<term>Lung (metabolism)</term>
<term>Macrophages (drug effects)</term>
<term>Macrophages (immunology)</term>
<term>Macrophages (metabolism)</term>
<term>Mice (MeSH)</term>
<term>Mice, Knockout (MeSH)</term>
<term>NF-kappa B (metabolism)</term>
<term>RAW 264.7 Cells (MeSH)</term>
<term>RNA, Messenger (genetics)</term>
<term>RNA, Messenger (metabolism)</term>
<term>RNA, Small Interfering (genetics)</term>
<term>Signal Transduction (MeSH)</term>
<term>TNF Receptor-Associated Factor 6 (metabolism)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>ARN messager (génétique)</term>
<term>ARN messager (métabolisme)</term>
<term>Allergènes (administration et posologie)</term>
<term>Animaux (MeSH)</term>
<term>Asthme (immunologie)</term>
<term>Asthme (métabolisme)</term>
<term>Asthme (étiologie)</term>
<term>Cellules RAW 264.7 (MeSH)</term>
<term>Expression des gènes (effets des médicaments et des substances chimiques)</term>
<term>Facteur de transcription NF-kappa B (métabolisme)</term>
<term>Facteur-6 associé aux récepteurs de TNF (métabolisme)</term>
<term>Glutarédoxines (déficit)</term>
<term>Glutarédoxines (génétique)</term>
<term>Glutarédoxines (métabolisme)</term>
<term>Glutathion (métabolisme)</term>
<term>Interleukine-33 (biosynthèse)</term>
<term>Interleukine-33 (génétique)</term>
<term>Lipopolysaccharides (pharmacologie)</term>
<term>Macrophages (effets des médicaments et des substances chimiques)</term>
<term>Macrophages (immunologie)</term>
<term>Macrophages (métabolisme)</term>
<term>Modèles animaux de maladie humaine (MeSH)</term>
<term>Petit ARN interférent (génétique)</term>
<term>Poumon (immunologie)</term>
<term>Poumon (métabolisme)</term>
<term>Souris (MeSH)</term>
<term>Souris knockout (MeSH)</term>
<term>Techniques de knock-down de gènes (MeSH)</term>
<term>Transduction du signal (MeSH)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Allergens</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Interleukin-33</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="deficiency" xml:lang="en"><term>Glutaredoxins</term>
</keywords>
<keywords scheme="MESH" qualifier="administration et posologie" xml:lang="fr"><term>Allergènes</term>
</keywords>
<keywords scheme="MESH" qualifier="biosynthèse" xml:lang="fr"><term>Interleukine-33</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Gene Expression</term>
<term>Macrophages</term>
</keywords>
<keywords scheme="MESH" qualifier="déficit" xml:lang="fr"><term>Glutarédoxines</term>
</keywords>
<keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Expression des gènes</term>
<term>Macrophages</term>
</keywords>
<keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Asthma</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Glutaredoxins</term>
<term>Interleukin-33</term>
<term>RNA, Messenger</term>
<term>RNA, Small Interfering</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>ARN messager</term>
<term>Glutarédoxines</term>
<term>Interleukine-33</term>
<term>Petit ARN interférent</term>
</keywords>
<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Asthme</term>
<term>Macrophages</term>
<term>Poumon</term>
</keywords>
<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Asthma</term>
<term>Lung</term>
<term>Macrophages</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Asthma</term>
<term>Glutaredoxins</term>
<term>Glutathione</term>
<term>Lung</term>
<term>Macrophages</term>
<term>NF-kappa B</term>
<term>RNA, Messenger</term>
<term>TNF Receptor-Associated Factor 6</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>ARN messager</term>
<term>Asthme</term>
<term>Facteur de transcription NF-kappa B</term>
<term>Facteur-6 associé aux récepteurs de TNF</term>
<term>Glutarédoxines</term>
<term>Glutathion</term>
<term>Macrophages</term>
<term>Poumon</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Lipopolysaccharides</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Lipopolysaccharides</term>
</keywords>
<keywords scheme="MESH" qualifier="étiologie" xml:lang="fr"><term>Asthme</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Disease Models, Animal</term>
<term>Gene Knockdown Techniques</term>
<term>Mice</term>
<term>Mice, Knockout</term>
<term>RAW 264.7 Cells</term>
<term>Signal Transduction</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Cellules RAW 264.7</term>
<term>Modèles animaux de maladie humaine</term>
<term>Souris</term>
<term>Souris knockout</term>
<term>Techniques de knock-down de gènes</term>
<term>Transduction du signal</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">Interleukin (IL)-33 is an interleukin-1 like cytokine that enhances Th2 responses and mediates mucosal immunity and allergic inflammation but the mechanism regulating endogenous IL-33 production are still under investigation. In macrophages, lipopolysaccharide (LPS) administration resulted in marked induction of IL-33 mRNA that was blunted in macrophages from glutaredoxin-1 (Glrx) knockout mice and in RAW264.7 macrophages with Glrx knockdown by siRNA. Glutaredoxin-1 is a small cytosolic thioltransferase that controls a reversible protein thiol modification, S-glutationylation (protein-GSH adducts), thereby regulating redox signaling. In this study, we examined the mechanism of Glrx regulation of endogenous IL-33 induction in macrophages. Glrx knockdown resulted in impaired de-glutathionylation of TRAF6, which is required for TRAF6 activation, and inhibited downstream IKKβ and NF-κB activation. Inhibitors of NF-κB suppressed IL-33 induction and chromatin IP sequencing data analysis confirmed that IL-33 is an NF-κB-responsive gene. Since TRAF6-NF-κB activation is also essential for IL-33 signaling through its receptor, ST2L, we next tested the involvement of Glrx in exogenous IL-33 responses in RAW264.7 cells. Recombinant IL-33 (rIL-33) administration induced IL-33 mRNA expression in RAW264.7 macrophages, and this was inhibited by Glrx knockdown. Interestingly, rIL-33-induced IL-33 protein was identified as the 20 kDa cleaved form whereas LPS-induced IL-33 protein was identified as full-length IL-33, which may be less active than the cleaved form. In a clinically-relevant mouse model of asthma, intra-tracheal cockroach antigen treatment induced Glrx protein in wild type mouse lungs but Glrx induction was attenuated in IL-33 knockout mouse lungs, suggesting that IL-33 may regulate Glrx induction in vivo in response to allergen challenge. In summary, our data reveal a novel mechanism by which Glrx controls both LPS- and IL-33-mediated NF-κB activation leading to IL-33 production, and paracrine IL-33 can induce Glrx to further regulate inflammatory reactions.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">30682073</PMID>
<DateCompleted><Year>2019</Year>
<Month>10</Month>
<Day>22</Day>
</DateCompleted>
<DateRevised><Year>2020</Year>
<Month>03</Month>
<Day>09</Day>
</DateRevised>
<Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Electronic">1932-6203</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>14</Volume>
<Issue>1</Issue>
<PubDate><Year>2019</Year>
</PubDate>
</JournalIssue>
<Title>PloS one</Title>
<ISOAbbreviation>PLoS One</ISOAbbreviation>
</Journal>
<ArticleTitle>IL-33 induction and signaling are controlled by glutaredoxin-1 in mouse macrophages.</ArticleTitle>
<Pagination><MedlinePgn>e0210827</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1371/journal.pone.0210827</ELocationID>
<Abstract><AbstractText>Interleukin (IL)-33 is an interleukin-1 like cytokine that enhances Th2 responses and mediates mucosal immunity and allergic inflammation but the mechanism regulating endogenous IL-33 production are still under investigation. In macrophages, lipopolysaccharide (LPS) administration resulted in marked induction of IL-33 mRNA that was blunted in macrophages from glutaredoxin-1 (Glrx) knockout mice and in RAW264.7 macrophages with Glrx knockdown by siRNA. Glutaredoxin-1 is a small cytosolic thioltransferase that controls a reversible protein thiol modification, S-glutationylation (protein-GSH adducts), thereby regulating redox signaling. In this study, we examined the mechanism of Glrx regulation of endogenous IL-33 induction in macrophages. Glrx knockdown resulted in impaired de-glutathionylation of TRAF6, which is required for TRAF6 activation, and inhibited downstream IKKβ and NF-κB activation. Inhibitors of NF-κB suppressed IL-33 induction and chromatin IP sequencing data analysis confirmed that IL-33 is an NF-κB-responsive gene. Since TRAF6-NF-κB activation is also essential for IL-33 signaling through its receptor, ST2L, we next tested the involvement of Glrx in exogenous IL-33 responses in RAW264.7 cells. Recombinant IL-33 (rIL-33) administration induced IL-33 mRNA expression in RAW264.7 macrophages, and this was inhibited by Glrx knockdown. Interestingly, rIL-33-induced IL-33 protein was identified as the 20 kDa cleaved form whereas LPS-induced IL-33 protein was identified as full-length IL-33, which may be less active than the cleaved form. In a clinically-relevant mouse model of asthma, intra-tracheal cockroach antigen treatment induced Glrx protein in wild type mouse lungs but Glrx induction was attenuated in IL-33 knockout mouse lungs, suggesting that IL-33 may regulate Glrx induction in vivo in response to allergen challenge. In summary, our data reveal a novel mechanism by which Glrx controls both LPS- and IL-33-mediated NF-κB activation leading to IL-33 production, and paracrine IL-33 can induce Glrx to further regulate inflammatory reactions.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Weinberg</LastName>
<ForeName>Ellen O</ForeName>
<Initials>EO</Initials>
<AffiliationInfo><Affiliation>Department of Medicine, Section of Infectious Diseases, Boston University School of Medicine, Boston, Massachusetts, United States of America.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Ferran</LastName>
<ForeName>Beatriz</ForeName>
<Initials>B</Initials>
<AffiliationInfo><Affiliation>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, United States of America.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Tsukahara</LastName>
<ForeName>Yuko</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, United States of America.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Hatch</LastName>
<ForeName>Michaela M S</ForeName>
<Initials>MMS</Initials>
<AffiliationInfo><Affiliation>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, United States of America.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Han</LastName>
<ForeName>Jingyan</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, United States of America.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Murdoch</LastName>
<ForeName>Colin E</ForeName>
<Initials>CE</Initials>
<AffiliationInfo><Affiliation>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, United States of America.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Matsui</LastName>
<ForeName>Reiko</ForeName>
<Initials>R</Initials>
<Identifier Source="ORCID">0000-0002-8132-2823</Identifier>
<AffiliationInfo><Affiliation>Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, United States of America.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><GrantID>R21 NS108724</GrantID>
<Acronym>NS</Acronym>
<Agency>NINDS NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>T32 HL007224</GrantID>
<Acronym>HL</Acronym>
<Agency>NHLBI NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R01 HL133013</GrantID>
<Acronym>HL</Acronym>
<Agency>NHLBI NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R03 AI090404</GrantID>
<Acronym>AI</Acronym>
<Agency>NIAID NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R03 AG051857</GrantID>
<Acronym>AG</Acronym>
<Agency>NIA NIH HHS</Agency>
<Country>United States</Country>
</Grant>
</GrantList>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
<PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2019</Year>
<Month>01</Month>
<Day>25</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>United States</Country>
<MedlineTA>PLoS One</MedlineTA>
<NlmUniqueID>101285081</NlmUniqueID>
<ISSNLinking>1932-6203</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000485">Allergens</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C516006">Glrx protein, mouse</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D054477">Glutaredoxins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C506535">Il33 protein, mouse</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000067596">Interleukin-33</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D008070">Lipopolysaccharides</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D016328">NF-kappa B</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D012333">RNA, Messenger</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D034741">RNA, Small Interfering</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D048029">TNF Receptor-Associated Factor 6</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C000631106">TRAF6 protein, mouse</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C060835">allergen CRa, cockroach</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>GAN16C9B8O</RegistryNumber>
<NameOfSubstance UI="D005978">Glutathione</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D000485" MajorTopicYN="N">Allergens</DescriptorName>
<QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D001249" MajorTopicYN="N">Asthma</DescriptorName>
<QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015870" MajorTopicYN="N">Gene Expression</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D055785" MajorTopicYN="N">Gene Knockdown Techniques</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D054477" MajorTopicYN="N">Glutaredoxins</DescriptorName>
<QualifierName UI="Q000172" MajorTopicYN="N">deficiency</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005978" MajorTopicYN="N">Glutathione</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000067596" MajorTopicYN="N">Interleukin-33</DescriptorName>
<QualifierName UI="Q000096" MajorTopicYN="Y">biosynthesis</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008070" MajorTopicYN="N">Lipopolysaccharides</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008168" MajorTopicYN="N">Lung</DescriptorName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008264" MajorTopicYN="N">Macrophages</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
<QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018345" MajorTopicYN="N">Mice, Knockout</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D016328" MajorTopicYN="N">NF-kappa B</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000067996" MajorTopicYN="N">RAW 264.7 Cells</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D012333" MajorTopicYN="N">RNA, Messenger</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D034741" MajorTopicYN="N">RNA, Small Interfering</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D048029" MajorTopicYN="N">TNF Receptor-Associated Factor 6</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
</MeshHeadingList>
<CoiStatement>The authors have declared that no competing interests exist.</CoiStatement>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2018</Year>
<Month>08</Month>
<Day>31</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted"><Year>2019</Year>
<Month>01</Month>
<Day>02</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="entrez"><Year>2019</Year>
<Month>1</Month>
<Day>26</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="pubmed"><Year>2019</Year>
<Month>1</Month>
<Day>27</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="medline"><Year>2019</Year>
<Month>10</Month>
<Day>23</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
</History>
<PublicationStatus>epublish</PublicationStatus>
<ArticleIdList><ArticleId IdType="pubmed">30682073</ArticleId>
<ArticleId IdType="doi">10.1371/journal.pone.0210827</ArticleId>
<ArticleId IdType="pii">PONE-D-18-25658</ArticleId>
<ArticleId IdType="pmc">PMC6347181</ArticleId>
</ArticleIdList>
<ReferenceList><Reference><Citation>J Immunol. 2009 Nov 15;183(10):6469-77</Citation>
<ArticleIdList><ArticleId IdType="pubmed">19841166</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Free Radic Biol Med. 2007 Nov 1;43(9):1299-312</Citation>
<ArticleIdList><ArticleId IdType="pubmed">17893043</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Am J Respir Cell Mol Biol. 2007 Feb;36(2):147-51</Citation>
<ArticleIdList><ArticleId IdType="pubmed">16980552</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Am J Pathol. 2008 Oct;173(4):1229-42</Citation>
<ArticleIdList><ArticleId IdType="pubmed">18787100</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Proc Natl Acad Sci U S A. 2010 Oct 26;107(43):18581-6</Citation>
<ArticleIdList><ArticleId IdType="pubmed">20937871</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Eur J Pharmacol. 2018 Jan 5;818:235-240</Citation>
<ArticleIdList><ArticleId IdType="pubmed">29107673</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>PLoS One. 2011 Apr 11;6(4):e18404</Citation>
<ArticleIdList><ArticleId IdType="pubmed">21494550</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Eur J Immunol. 2001 Oct;31(10):2979-85</Citation>
<ArticleIdList><ArticleId IdType="pubmed">11592074</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Am J Respir Cell Mol Biol. 2016 Sep;55(3):377-86</Citation>
<ArticleIdList><ArticleId IdType="pubmed">27035878</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Immunol. 2009 Dec 15;183(12):7890-7</Citation>
<ArticleIdList><ArticleId IdType="pubmed">19933859</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Immunol. 2013 May 1;190(9):4489-99</Citation>
<ArticleIdList><ArticleId IdType="pubmed">23547117</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Immunol. 2011 Apr 1;186(7):4375-87</Citation>
<ArticleIdList><ArticleId IdType="pubmed">21357533</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Mol Cells. 2008 May 31;25(3):332-46</Citation>
<ArticleIdList><ArticleId IdType="pubmed">18483468</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Immunol. 2004 Sep 1;173(5):2913-7</Citation>
<ArticleIdList><ArticleId IdType="pubmed">15322147</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Curr Protoc Immunol. 2008 Nov;Chapter 14:Unit 14.1</Citation>
<ArticleIdList><ArticleId IdType="pubmed">19016445</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>PLoS One. 2016 Jun 16;11(6):e0157571</Citation>
<ArticleIdList><ArticleId IdType="pubmed">27310495</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Free Radic Biol Med. 2011 Sep 15;51(6):1249-57</Citation>
<ArticleIdList><ArticleId IdType="pubmed">21762778</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Am J Respir Cell Mol Biol. 2011 Nov;45(5):931-7</Citation>
<ArticleIdList><ArticleId IdType="pubmed">21454804</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Genes Dev. 2010 Dec 15;24(24):2760-5</Citation>
<ArticleIdList><ArticleId IdType="pubmed">21106671</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Respir Res. 2018 Mar 27;19(1):52</Citation>
<ArticleIdList><ArticleId IdType="pubmed">29587772</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Immunol. 2011 Aug 15;187(4):1609-16</Citation>
<ArticleIdList><ArticleId IdType="pubmed">21734074</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Biol Chem. 2014 Mar 21;289(12):8633-44</Citation>
<ArticleIdList><ArticleId IdType="pubmed">24482236</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Biol Chem. 2009 Jul 17;284(29):19420-6</Citation>
<ArticleIdList><ArticleId IdType="pubmed">19465481</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Am J Respir Cell Mol Biol. 2011 Apr;44(4):491-9</Citation>
<ArticleIdList><ArticleId IdType="pubmed">20539014</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Biochem Soc Trans. 2014 Dec;42(6):1665-70</Citation>
<ArticleIdList><ArticleId IdType="pubmed">25399587</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Biochemistry. 2001 Nov 27;40(47):14134-42</Citation>
<ArticleIdList><ArticleId IdType="pubmed">11714266</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Proc Natl Acad Sci U S A. 2003 Apr 29;100(9):5103-6</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12697895</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cell Signal. 2008 Sep;20(9):1679-86</Citation>
<ArticleIdList><ArticleId IdType="pubmed">18603409</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Invest Ophthalmol Vis Sci. 2010 Mar;51(3):1524-32</Citation>
<ArticleIdList><ArticleId IdType="pubmed">19892870</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>PLoS One. 2008 Oct 06;3(10):e3331</Citation>
<ArticleIdList><ArticleId IdType="pubmed">18836528</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Methods Mol Biol. 2017;1559:121-136</Citation>
<ArticleIdList><ArticleId IdType="pubmed">28063042</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Proc Natl Acad Sci U S A. 2012 Jan 31;109(5):1673-8</Citation>
<ArticleIdList><ArticleId IdType="pubmed">22307629</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Proc Natl Acad Sci U S A. 2007 Jan 2;104(1):282-7</Citation>
<ArticleIdList><ArticleId IdType="pubmed">17185418</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Sci Rep. 2016 Oct 03;6:34255</Citation>
<ArticleIdList><ArticleId IdType="pubmed">27694941</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Proc Natl Acad Sci U S A. 2014 Oct 28;111(43):15502-7</Citation>
<ArticleIdList><ArticleId IdType="pubmed">25313073</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Immunology. 2010 Jun;130(2):172-80</Citation>
<ArticleIdList><ArticleId IdType="pubmed">20070408</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Sci Rep. 2017 Jun 26;7(1):4219</Citation>
<ArticleIdList><ArticleId IdType="pubmed">28652606</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Science. 2012 Feb 24;335(6071):984-9</Citation>
<ArticleIdList><ArticleId IdType="pubmed">22323740</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Proc Natl Acad Sci U S A. 2006 Aug 29;103(35):13086-91</Citation>
<ArticleIdList><ArticleId IdType="pubmed">16916935</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Biochemistry. 2000 Sep 12;39(36):11121-8</Citation>
<ArticleIdList><ArticleId IdType="pubmed">10998251</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Mol Immunol. 2017 Oct;90:42-49</Citation>
<ArticleIdList><ArticleId IdType="pubmed">28697404</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Blood. 2009 Oct 1;114(14):3117-26</Citation>
<ArticleIdList><ArticleId IdType="pubmed">19661270</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Gene. 1997 Sep 15;197(1-2):189-93</Citation>
<ArticleIdList><ArticleId IdType="pubmed">9332366</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Biochem Biophys Res Commun. 2010 Dec 17;403(3-4):335-9</Citation>
<ArticleIdList><ArticleId IdType="pubmed">21078302</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Allergy Asthma Immunol Res. 2011 Apr;3(2):81-8</Citation>
<ArticleIdList><ArticleId IdType="pubmed">21461246</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Proc Natl Acad Sci U S A. 2009 Jun 2;106(22):9021-6</Citation>
<ArticleIdList><ArticleId IdType="pubmed">19439663</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Immunity. 2005 Nov;23(5):479-90</Citation>
<ArticleIdList><ArticleId IdType="pubmed">16286016</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Nat Commun. 2015 Sep 14;6:8327</Citation>
<ArticleIdList><ArticleId IdType="pubmed">26365875</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Clin Invest. 2013 May;123(5):2287-97</Citation>
<ArticleIdList><ArticleId IdType="pubmed">23585480</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
</PubmedData>
</pubmed>
<affiliations><list><country><li>États-Unis</li>
</country>
<region><li>Massachusetts</li>
</region>
</list>
<tree><country name="États-Unis"><region name="Massachusetts"><name sortKey="Weinberg, Ellen O" sort="Weinberg, Ellen O" uniqKey="Weinberg E" first="Ellen O" last="Weinberg">Ellen O. Weinberg</name>
</region>
<name sortKey="Ferran, Beatriz" sort="Ferran, Beatriz" uniqKey="Ferran B" first="Beatriz" last="Ferran">Beatriz Ferran</name>
<name sortKey="Han, Jingyan" sort="Han, Jingyan" uniqKey="Han J" first="Jingyan" last="Han">Jingyan Han</name>
<name sortKey="Hatch, Michaela M S" sort="Hatch, Michaela M S" uniqKey="Hatch M" first="Michaela M S" last="Hatch">Michaela M S. Hatch</name>
<name sortKey="Matsui, Reiko" sort="Matsui, Reiko" uniqKey="Matsui R" first="Reiko" last="Matsui">Reiko Matsui</name>
<name sortKey="Murdoch, Colin E" sort="Murdoch, Colin E" uniqKey="Murdoch C" first="Colin E" last="Murdoch">Colin E. Murdoch</name>
<name sortKey="Tsukahara, Yuko" sort="Tsukahara, Yuko" uniqKey="Tsukahara Y" first="Yuko" last="Tsukahara">Yuko Tsukahara</name>
</country>
</tree>
</affiliations>
</record>
Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Bois/explor/GlutaredoxinV1/Data/Main/Exploration
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000156 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd -nk 000156 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien |wiki= Bois |area= GlutaredoxinV1 |flux= Main |étape= Exploration |type= RBID |clé= pubmed:30682073 |texte= IL-33 induction and signaling are controlled by glutaredoxin-1 in mouse macrophages. }}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Exploration/RBID.i -Sk "pubmed:30682073" \ | HfdSelect -Kh $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd \ | NlmPubMed2Wicri -a GlutaredoxinV1
This area was generated with Dilib version V0.6.37. |