Serveur d'exploration sur la glutarédoxine

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Ablation of Glutaredoxin-1 Modulates House Dust Mite-Induced Allergic Airways Disease in Mice.

Identifieur interne : 000480 ( Main/Exploration ); précédent : 000479; suivant : 000481

Ablation of Glutaredoxin-1 Modulates House Dust Mite-Induced Allergic Airways Disease in Mice.

Auteurs : Sidra M. Hoffman ; Xi Qian ; James D. Nolin ; David G. Chapman [États-Unis] ; Shi Biao Chia ; Karolyn G. Lahue ; Robert Schneider ; Jennifer L. Ather [États-Unis] ; Matthew J. Randall [États-Unis] ; David H. Mcmillan ; Jane T. Jones ; Douglas J. Taatjes ; Minara Aliyeva [États-Unis] ; Nirav Daphtary [États-Unis] ; Sarah Abdalla ; Lennart K A. Lundblad [États-Unis] ; Ye-Shih Ho ; Vikas Anathy ; Charles G. Irvin [États-Unis] ; Emiel F M. Wouters [Pays-Bas] ; Niki L. Reynaert [Pays-Bas] ; Anne E. Dixon [États-Unis] ; Albert Van Der Vliet ; Matthew E. Poynter [États-Unis] ; Yvonne M W. Janssen-Heininger

Source :

RBID : pubmed:27035878

Descripteurs français

English descriptors

Abstract

Protein S-glutathionylation (PSSG) is an oxidant-induced post-translational modification of protein cysteines that impacts structure and function. The oxidoreductase glutaredoxin-1 (Glrx1) under physiological conditions catalyzes deglutathionylation and restores the protein thiol group. The involvement of Glrx1/PSSG in allergic inflammation induced by asthma-relevant allergens remains unknown. In the present study, we examined the impact of genetic ablation of Glrx1 in the pathogenesis of house dust mite (HDM)-induced allergic airways disease in mice. Wild-type (WT) or Glrx1(-/-) mice were instilled intranasally with HDM on 5 consecutive days for 3 weeks. As expected, overall PSSG was increased in Glrx1(-/-) HDM mice as compared with WT animals. Total cells in bronchoalveolar lavage fluid were similarly increased in HDM-treated WT and Glrx1(-/-) mice. However, in response to HDM, mice lacking Glrx1 demonstrated significantly more neutrophils and macrophages but fewer eosinophils as compared with HDM-exposed WT mice. mRNA expression of the Th2-associated cytokines IL-13 and IL-6, as well as mucin-5AC (Muc5ac), was significantly attenuated in Glrx1(-/-) HDM-treated mice. Conversely, mRNA expression of IFN-γ and IL-17A was increased in Glrx1(-/-) HDM mice compared with WT littermates. Restimulation of single-cell suspensions isolated from lungs or spleens with HDM resulted in enhanced IL-17A and decreased IL-5 production in cells derived from inflamed Glrx1(-/-) mice compared with WT animals. Finally, HDM-induced tissue damping and elastance were significantly attenuated in Glrx1(-/-) mice compared with WT littermates. These results demonstrate that the Glrx1-PSSG axis plays a pivotal role in HDM-induced allergic airways disease in association with enhanced type 2 inflammation and restriction of IFN-γ and IL-17A.

DOI: 10.1165/rcmb.2015-0401OC
PubMed: 27035878
PubMed Central: PMC5023028


Affiliations:


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<name sortKey="Jones, Jane T" sort="Jones, Jane T" uniqKey="Jones J" first="Jane T" last="Jones">Jane T. Jones</name>
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<name sortKey="Irvin, Charles G" sort="Irvin, Charles G" uniqKey="Irvin C" first="Charles G" last="Irvin">Charles G. Irvin</name>
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<name sortKey="Reynaert, Niki L" sort="Reynaert, Niki L" uniqKey="Reynaert N" first="Niki L" last="Reynaert">Niki L. Reynaert</name>
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<name sortKey="Dixon, Anne E" sort="Dixon, Anne E" uniqKey="Dixon A" first="Anne E" last="Dixon">Anne E. Dixon</name>
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<name sortKey="Poynter, Matthew E" sort="Poynter, Matthew E" uniqKey="Poynter M" first="Matthew E" last="Poynter">Matthew E. Poynter</name>
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<title xml:lang="en">Ablation of Glutaredoxin-1 Modulates House Dust Mite-Induced Allergic Airways Disease in Mice.</title>
<author>
<name sortKey="Hoffman, Sidra M" sort="Hoffman, Sidra M" uniqKey="Hoffman S" first="Sidra M" last="Hoffman">Sidra M. Hoffman</name>
<affiliation>
<nlm:affiliation>Departments of 1 Pathology and Laboratory Medicine and.</nlm:affiliation>
<wicri:noCountry code="no comma">Departments of 1 Pathology and Laboratory Medicine and.</wicri:noCountry>
</affiliation>
</author>
<author>
<name sortKey="Qian, Xi" sort="Qian, Xi" uniqKey="Qian X" first="Xi" last="Qian">Xi Qian</name>
<affiliation>
<nlm:affiliation>Departments of 1 Pathology and Laboratory Medicine and.</nlm:affiliation>
<wicri:noCountry code="no comma">Departments of 1 Pathology and Laboratory Medicine and.</wicri:noCountry>
</affiliation>
</author>
<author>
<name sortKey="Nolin, James D" sort="Nolin, James D" uniqKey="Nolin J" first="James D" last="Nolin">James D. Nolin</name>
<affiliation>
<nlm:affiliation>Departments of 1 Pathology and Laboratory Medicine and.</nlm:affiliation>
<wicri:noCountry code="no comma">Departments of 1 Pathology and Laboratory Medicine and.</wicri:noCountry>
</affiliation>
</author>
<author>
<name sortKey="Chapman, David G" sort="Chapman, David G" uniqKey="Chapman D" first="David G" last="Chapman">David G. Chapman</name>
<affiliation wicri:level="2">
<nlm:affiliation>2 Medicine, University of Vermont, Burlington, Vermont.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<placeName>
<region type="state">Vermont</region>
</placeName>
<wicri:cityArea>2 Medicine, University of Vermont, Burlington</wicri:cityArea>
</affiliation>
</author>
<author>
<name sortKey="Chia, Shi Biao" sort="Chia, Shi Biao" uniqKey="Chia S" first="Shi Biao" last="Chia">Shi Biao Chia</name>
<affiliation>
<nlm:affiliation>Departments of 1 Pathology and Laboratory Medicine and.</nlm:affiliation>
<wicri:noCountry code="no comma">Departments of 1 Pathology and Laboratory Medicine and.</wicri:noCountry>
</affiliation>
</author>
<author>
<name sortKey="Lahue, Karolyn G" sort="Lahue, Karolyn G" uniqKey="Lahue K" first="Karolyn G" last="Lahue">Karolyn G. Lahue</name>
<affiliation>
<nlm:affiliation>Departments of 1 Pathology and Laboratory Medicine and.</nlm:affiliation>
<wicri:noCountry code="no comma">Departments of 1 Pathology and Laboratory Medicine and.</wicri:noCountry>
</affiliation>
</author>
<author>
<name sortKey="Schneider, Robert" sort="Schneider, Robert" uniqKey="Schneider R" first="Robert" last="Schneider">Robert Schneider</name>
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<nlm:affiliation>Departments of 1 Pathology and Laboratory Medicine and.</nlm:affiliation>
<wicri:noCountry code="no comma">Departments of 1 Pathology and Laboratory Medicine and.</wicri:noCountry>
</affiliation>
</author>
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<name sortKey="Ather, Jennifer L" sort="Ather, Jennifer L" uniqKey="Ather J" first="Jennifer L" last="Ather">Jennifer L. Ather</name>
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</placeName>
<wicri:cityArea>2 Medicine, University of Vermont, Burlington</wicri:cityArea>
</affiliation>
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<name sortKey="Randall, Matthew J" sort="Randall, Matthew J" uniqKey="Randall M" first="Matthew J" last="Randall">Matthew J. Randall</name>
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<nlm:affiliation>2 Medicine, University of Vermont, Burlington, Vermont.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<placeName>
<region type="state">Vermont</region>
</placeName>
<wicri:cityArea>2 Medicine, University of Vermont, Burlington</wicri:cityArea>
</affiliation>
</author>
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<name sortKey="Mcmillan, David H" sort="Mcmillan, David H" uniqKey="Mcmillan D" first="David H" last="Mcmillan">David H. Mcmillan</name>
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<nlm:affiliation>Departments of 1 Pathology and Laboratory Medicine and.</nlm:affiliation>
<wicri:noCountry code="no comma">Departments of 1 Pathology and Laboratory Medicine and.</wicri:noCountry>
</affiliation>
</author>
<author>
<name sortKey="Jones, Jane T" sort="Jones, Jane T" uniqKey="Jones J" first="Jane T" last="Jones">Jane T. Jones</name>
<affiliation>
<nlm:affiliation>Departments of 1 Pathology and Laboratory Medicine and.</nlm:affiliation>
<wicri:noCountry code="no comma">Departments of 1 Pathology and Laboratory Medicine and.</wicri:noCountry>
</affiliation>
</author>
<author>
<name sortKey="Taatjes, Douglas J" sort="Taatjes, Douglas J" uniqKey="Taatjes D" first="Douglas J" last="Taatjes">Douglas J. Taatjes</name>
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<wicri:noCountry code="no comma">Departments of 1 Pathology and Laboratory Medicine and.</wicri:noCountry>
</affiliation>
</author>
<author>
<name sortKey="Aliyeva, Minara" sort="Aliyeva, Minara" uniqKey="Aliyeva M" first="Minara" last="Aliyeva">Minara Aliyeva</name>
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<nlm:affiliation>2 Medicine, University of Vermont, Burlington, Vermont.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<placeName>
<region type="state">Vermont</region>
</placeName>
<wicri:cityArea>2 Medicine, University of Vermont, Burlington</wicri:cityArea>
</affiliation>
</author>
<author>
<name sortKey="Daphtary, Nirav" sort="Daphtary, Nirav" uniqKey="Daphtary N" first="Nirav" last="Daphtary">Nirav Daphtary</name>
<affiliation wicri:level="2">
<nlm:affiliation>2 Medicine, University of Vermont, Burlington, Vermont.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<placeName>
<region type="state">Vermont</region>
</placeName>
<wicri:cityArea>2 Medicine, University of Vermont, Burlington</wicri:cityArea>
</affiliation>
</author>
<author>
<name sortKey="Abdalla, Sarah" sort="Abdalla, Sarah" uniqKey="Abdalla S" first="Sarah" last="Abdalla">Sarah Abdalla</name>
<affiliation>
<nlm:affiliation>Departments of 1 Pathology and Laboratory Medicine and.</nlm:affiliation>
<wicri:noCountry code="no comma">Departments of 1 Pathology and Laboratory Medicine and.</wicri:noCountry>
</affiliation>
</author>
<author>
<name sortKey="Lundblad, Lennart K A" sort="Lundblad, Lennart K A" uniqKey="Lundblad L" first="Lennart K A" last="Lundblad">Lennart K A. Lundblad</name>
<affiliation wicri:level="2">
<nlm:affiliation>2 Medicine, University of Vermont, Burlington, Vermont.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<placeName>
<region type="state">Vermont</region>
</placeName>
<wicri:cityArea>2 Medicine, University of Vermont, Burlington</wicri:cityArea>
</affiliation>
</author>
<author>
<name sortKey="Ho, Ye Shih" sort="Ho, Ye Shih" uniqKey="Ho Y" first="Ye-Shih" last="Ho">Ye-Shih Ho</name>
<affiliation>
<nlm:affiliation>3 Institute of Environmental Health Sciences, Wayne State University, Detroit, Michigan; and.</nlm:affiliation>
<wicri:noCountry code="subField">Michigan; and</wicri:noCountry>
</affiliation>
</author>
<author>
<name sortKey="Anathy, Vikas" sort="Anathy, Vikas" uniqKey="Anathy V" first="Vikas" last="Anathy">Vikas Anathy</name>
<affiliation>
<nlm:affiliation>Departments of 1 Pathology and Laboratory Medicine and.</nlm:affiliation>
<wicri:noCountry code="no comma">Departments of 1 Pathology and Laboratory Medicine and.</wicri:noCountry>
</affiliation>
</author>
<author>
<name sortKey="Irvin, Charles G" sort="Irvin, Charles G" uniqKey="Irvin C" first="Charles G" last="Irvin">Charles G. Irvin</name>
<affiliation wicri:level="2">
<nlm:affiliation>2 Medicine, University of Vermont, Burlington, Vermont.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<placeName>
<region type="state">Vermont</region>
</placeName>
<wicri:cityArea>2 Medicine, University of Vermont, Burlington</wicri:cityArea>
</affiliation>
</author>
<author>
<name sortKey="Wouters, Emiel F M" sort="Wouters, Emiel F M" uniqKey="Wouters E" first="Emiel F M" last="Wouters">Emiel F M. Wouters</name>
<affiliation wicri:level="1">
<nlm:affiliation>4 Department of Respiratory Medicine, Maastricht University Medical Center, Maastricht, the Netherlands.</nlm:affiliation>
<country xml:lang="fr" wicri:curation="lc">Pays-Bas</country>
<wicri:regionArea>4 Department of Respiratory Medicine, Maastricht University Medical Center, Maastricht</wicri:regionArea>
<wicri:noRegion>Maastricht</wicri:noRegion>
</affiliation>
</author>
<author>
<name sortKey="Reynaert, Niki L" sort="Reynaert, Niki L" uniqKey="Reynaert N" first="Niki L" last="Reynaert">Niki L. Reynaert</name>
<affiliation wicri:level="1">
<nlm:affiliation>4 Department of Respiratory Medicine, Maastricht University Medical Center, Maastricht, the Netherlands.</nlm:affiliation>
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<name sortKey="Poynter, Matthew E" sort="Poynter, Matthew E" uniqKey="Poynter M" first="Matthew E" last="Poynter">Matthew E. Poynter</name>
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<title level="j">American journal of respiratory cell and molecular biology</title>
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<term>Animals (MeSH)</term>
<term>Cytokines (genetics)</term>
<term>Cytokines (metabolism)</term>
<term>Glutaredoxins (metabolism)</term>
<term>Glutathione (metabolism)</term>
<term>Hyperplasia (MeSH)</term>
<term>Hypersensitivity (blood)</term>
<term>Hypersensitivity (complications)</term>
<term>Hypersensitivity (parasitology)</term>
<term>Hypersensitivity (pathology)</term>
<term>Immunoglobulin E (blood)</term>
<term>Immunoglobulin G (blood)</term>
<term>Lung (parasitology)</term>
<term>Lung (pathology)</term>
<term>Mice, Inbred BALB C (MeSH)</term>
<term>Mucus (metabolism)</term>
<term>Pneumonia (blood)</term>
<term>Pneumonia (complications)</term>
<term>Pneumonia (parasitology)</term>
<term>Pneumonia (pathology)</term>
<term>Pyroglyphidae (physiology)</term>
<term>RNA, Messenger (genetics)</term>
<term>RNA, Messenger (metabolism)</term>
<term>Respiratory Hypersensitivity (blood)</term>
<term>Respiratory Hypersensitivity (parasitology)</term>
<term>Respiratory Hypersensitivity (pathology)</term>
<term>Respiratory Hypersensitivity (physiopathology)</term>
<term>Respiratory Mechanics (MeSH)</term>
<term>Th2 Cells (immunology)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr">
<term>ARN messager (génétique)</term>
<term>ARN messager (métabolisme)</term>
<term>Animaux (MeSH)</term>
<term>Cytokines (génétique)</term>
<term>Cytokines (métabolisme)</term>
<term>Glutarédoxines (métabolisme)</term>
<term>Glutathion (métabolisme)</term>
<term>Hyperplasie (MeSH)</term>
<term>Hypersensibilité (anatomopathologie)</term>
<term>Hypersensibilité (complications)</term>
<term>Hypersensibilité (parasitologie)</term>
<term>Hypersensibilité (sang)</term>
<term>Hypersensibilité respiratoire (anatomopathologie)</term>
<term>Hypersensibilité respiratoire (parasitologie)</term>
<term>Hypersensibilité respiratoire (physiopathologie)</term>
<term>Hypersensibilité respiratoire (sang)</term>
<term>Immunoglobuline E (sang)</term>
<term>Immunoglobuline G (sang)</term>
<term>Lymphocytes auxiliaires Th2 (immunologie)</term>
<term>Mucus (métabolisme)</term>
<term>Mécanique respiratoire (MeSH)</term>
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<term>Pneumopathie infectieuse (complications)</term>
<term>Pneumopathie infectieuse (parasitologie)</term>
<term>Pneumopathie infectieuse (sang)</term>
<term>Poumon (anatomopathologie)</term>
<term>Poumon (parasitologie)</term>
<term>Pyroglyphidae (physiologie)</term>
<term>Souris de lignée BALB C (MeSH)</term>
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<term>Immunoglobulin E</term>
<term>Immunoglobulin G</term>
</keywords>
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<term>Cytokines</term>
<term>RNA, Messenger</term>
</keywords>
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<term>Cytokines</term>
<term>Glutaredoxins</term>
<term>Glutathione</term>
<term>RNA, Messenger</term>
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<term>Hypersensibilité</term>
<term>Hypersensibilité respiratoire</term>
<term>Pneumopathie infectieuse</term>
<term>Poumon</term>
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<keywords scheme="MESH" qualifier="blood" xml:lang="en">
<term>Hypersensitivity</term>
<term>Pneumonia</term>
<term>Respiratory Hypersensitivity</term>
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<term>Hypersensitivity</term>
<term>Pneumonia</term>
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<term>ARN messager</term>
<term>Cytokines</term>
<term>Hypersensibilité</term>
<term>Pneumopathie infectieuse</term>
</keywords>
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<term>Lymphocytes auxiliaires Th2</term>
</keywords>
<keywords scheme="MESH" qualifier="immunology" xml:lang="en">
<term>Th2 Cells</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en">
<term>Mucus</term>
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<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr">
<term>ARN messager</term>
<term>Cytokines</term>
<term>Glutarédoxines</term>
<term>Glutathion</term>
<term>Mucus</term>
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<term>Hypersensibilité</term>
<term>Hypersensibilité respiratoire</term>
<term>Pneumopathie infectieuse</term>
<term>Poumon</term>
</keywords>
<keywords scheme="MESH" qualifier="parasitology" xml:lang="en">
<term>Hypersensitivity</term>
<term>Lung</term>
<term>Pneumonia</term>
<term>Respiratory Hypersensitivity</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en">
<term>Hypersensitivity</term>
<term>Lung</term>
<term>Pneumonia</term>
<term>Respiratory Hypersensitivity</term>
</keywords>
<keywords scheme="MESH" qualifier="physiologie" xml:lang="fr">
<term>Pyroglyphidae</term>
</keywords>
<keywords scheme="MESH" qualifier="physiology" xml:lang="en">
<term>Pyroglyphidae</term>
</keywords>
<keywords scheme="MESH" qualifier="physiopathologie" xml:lang="fr">
<term>Hypersensibilité respiratoire</term>
</keywords>
<keywords scheme="MESH" qualifier="physiopathology" xml:lang="en">
<term>Respiratory Hypersensitivity</term>
</keywords>
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<term>Hypersensibilité</term>
<term>Hypersensibilité respiratoire</term>
<term>Immunoglobuline E</term>
<term>Immunoglobuline G</term>
<term>Pneumopathie infectieuse</term>
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<term>Animals</term>
<term>Hyperplasia</term>
<term>Mice, Inbred BALB C</term>
<term>Respiratory Mechanics</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr">
<term>Animaux</term>
<term>Hyperplasie</term>
<term>Mécanique respiratoire</term>
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<div type="abstract" xml:lang="en">Protein S-glutathionylation (PSSG) is an oxidant-induced post-translational modification of protein cysteines that impacts structure and function. The oxidoreductase glutaredoxin-1 (Glrx1) under physiological conditions catalyzes deglutathionylation and restores the protein thiol group. The involvement of Glrx1/PSSG in allergic inflammation induced by asthma-relevant allergens remains unknown. In the present study, we examined the impact of genetic ablation of Glrx1 in the pathogenesis of house dust mite (HDM)-induced allergic airways disease in mice. Wild-type (WT) or Glrx1(-/-) mice were instilled intranasally with HDM on 5 consecutive days for 3 weeks. As expected, overall PSSG was increased in Glrx1(-/-) HDM mice as compared with WT animals. Total cells in bronchoalveolar lavage fluid were similarly increased in HDM-treated WT and Glrx1(-/-) mice. However, in response to HDM, mice lacking Glrx1 demonstrated significantly more neutrophils and macrophages but fewer eosinophils as compared with HDM-exposed WT mice. mRNA expression of the Th2-associated cytokines IL-13 and IL-6, as well as mucin-5AC (Muc5ac), was significantly attenuated in Glrx1(-/-) HDM-treated mice. Conversely, mRNA expression of IFN-γ and IL-17A was increased in Glrx1(-/-) HDM mice compared with WT littermates. Restimulation of single-cell suspensions isolated from lungs or spleens with HDM resulted in enhanced IL-17A and decreased IL-5 production in cells derived from inflamed Glrx1(-/-) mice compared with WT animals. Finally, HDM-induced tissue damping and elastance were significantly attenuated in Glrx1(-/-) mice compared with WT littermates. These results demonstrate that the Glrx1-PSSG axis plays a pivotal role in HDM-induced allergic airways disease in association with enhanced type 2 inflammation and restriction of IFN-γ and IL-17A.</div>
</front>
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<DateCompleted>
<Year>2017</Year>
<Month>06</Month>
<Day>30</Day>
</DateCompleted>
<DateRevised>
<Year>2018</Year>
<Month>11</Month>
<Day>13</Day>
</DateRevised>
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<Journal>
<ISSN IssnType="Electronic">1535-4989</ISSN>
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<Volume>55</Volume>
<Issue>3</Issue>
<PubDate>
<Year>2016</Year>
<Month>09</Month>
</PubDate>
</JournalIssue>
<Title>American journal of respiratory cell and molecular biology</Title>
<ISOAbbreviation>Am J Respir Cell Mol Biol</ISOAbbreviation>
</Journal>
<ArticleTitle>Ablation of Glutaredoxin-1 Modulates House Dust Mite-Induced Allergic Airways Disease in Mice.</ArticleTitle>
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<MedlinePgn>377-86</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1165/rcmb.2015-0401OC</ELocationID>
<Abstract>
<AbstractText>Protein S-glutathionylation (PSSG) is an oxidant-induced post-translational modification of protein cysteines that impacts structure and function. The oxidoreductase glutaredoxin-1 (Glrx1) under physiological conditions catalyzes deglutathionylation and restores the protein thiol group. The involvement of Glrx1/PSSG in allergic inflammation induced by asthma-relevant allergens remains unknown. In the present study, we examined the impact of genetic ablation of Glrx1 in the pathogenesis of house dust mite (HDM)-induced allergic airways disease in mice. Wild-type (WT) or Glrx1(-/-) mice were instilled intranasally with HDM on 5 consecutive days for 3 weeks. As expected, overall PSSG was increased in Glrx1(-/-) HDM mice as compared with WT animals. Total cells in bronchoalveolar lavage fluid were similarly increased in HDM-treated WT and Glrx1(-/-) mice. However, in response to HDM, mice lacking Glrx1 demonstrated significantly more neutrophils and macrophages but fewer eosinophils as compared with HDM-exposed WT mice. mRNA expression of the Th2-associated cytokines IL-13 and IL-6, as well as mucin-5AC (Muc5ac), was significantly attenuated in Glrx1(-/-) HDM-treated mice. Conversely, mRNA expression of IFN-γ and IL-17A was increased in Glrx1(-/-) HDM mice compared with WT littermates. Restimulation of single-cell suspensions isolated from lungs or spleens with HDM resulted in enhanced IL-17A and decreased IL-5 production in cells derived from inflamed Glrx1(-/-) mice compared with WT animals. Finally, HDM-induced tissue damping and elastance were significantly attenuated in Glrx1(-/-) mice compared with WT littermates. These results demonstrate that the Glrx1-PSSG axis plays a pivotal role in HDM-induced allergic airways disease in association with enhanced type 2 inflammation and restriction of IFN-γ and IL-17A.</AbstractText>
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