The thioredoxin-1 and glutathione/glutaredoxin-1 systems redundantly fuel murine B-cell development and responses.
Identifieur interne : 000108 ( Main/Exploration ); précédent : 000107; suivant : 000109The thioredoxin-1 and glutathione/glutaredoxin-1 systems redundantly fuel murine B-cell development and responses.
Auteurs : Jonathan Muri [Suisse] ; Helen Thut [Suisse] ; Sebastian Heer [Suisse] ; Caroline C. Krueger [Suisse] ; Georg W. Bornkamm [Allemagne] ; Martin F. Bachmann [Suisse] ; Manfred Kopf [Suisse]Source :
- European journal of immunology [ 1521-4141 ] ; 2019.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Centre germinatif (immunologie), Centre germinatif (métabolisme), Différenciation cellulaire (génétique), Différenciation cellulaire (immunologie), Glutarédoxines (génétique), Glutarédoxines (métabolisme), Lymphocytes B (cytologie), Lymphocytes B (immunologie), Lymphocytes B (métabolisme), Marqueurs biologiques (MeSH), Prolifération cellulaire (génétique), Souris (MeSH), Souris transgéniques (MeSH), Thiorédoxines (génétique), Thiorédoxines (métabolisme).
- MESH :
- cytologie : Lymphocytes B.
- génétique : Différenciation cellulaire, Glutarédoxines, Prolifération cellulaire, Thiorédoxines.
- immunologie : Centre germinatif, Différenciation cellulaire, Lymphocytes B.
- métabolisme : Centre germinatif, Glutarédoxines, Lymphocytes B, Thiorédoxines.
- Animaux, Marqueurs biologiques, Souris, Souris transgéniques.
English descriptors
- KwdEn :
- Animals (MeSH), B-Lymphocytes (cytology), B-Lymphocytes (immunology), B-Lymphocytes (metabolism), Biomarkers (MeSH), Cell Differentiation (genetics), Cell Differentiation (immunology), Cell Proliferation (genetics), Germinal Center (immunology), Germinal Center (metabolism), Glutaredoxins (genetics), Glutaredoxins (metabolism), Mice (MeSH), Mice, Transgenic (MeSH), Thioredoxins (genetics), Thioredoxins (metabolism).
- MESH :
- chemical , genetics : Glutaredoxins, Thioredoxins.
- chemical , metabolism : Glutaredoxins, Thioredoxins.
- chemical : Biomarkers.
- cytology : B-Lymphocytes.
- genetics : Cell Differentiation, Cell Proliferation.
- immunology : B-Lymphocytes, Cell Differentiation, Germinal Center.
- metabolism : B-Lymphocytes, Germinal Center.
- Animals, Mice, Mice, Transgenic.
Abstract
Antioxidant systems maintain cellular redox homeostasis. The thioredoxin-1 (Trx1) and the glutathione (GSH)/glutaredoxin-1 (Grx1) systems are key players in preserving cytosolic redox balance. In fact, T lymphocytes critically rely on reducing equivalents from the Trx1 system for DNA biosynthesis during metabolic reprogramming upon activation. We here show that the Trx1 system is also indispensable for development and functionality of marginal zone (MZ) B cells and B1 cells in mice. In contrast, development of conventional B cells, follicular B-cell homeostasis, germinal center reactions, and antibody responses are redundantly sustained by both antioxidant pathways. Proliferating B2 cells lacking Txnrd1 have increased glutathione (GSH) levels and upregulated cytosolic Grx1, which is barely detectable in expanding thymocytes. These results suggest that the redox capacity driving proliferation is more robust and flexible in B cells than in T cells, which may have profound implications for the therapy of B and T-cell neoplasms.
DOI: 10.1002/eji.201848044
PubMed: 30802940
Affiliations:
- Allemagne, Suisse
- Bavière, Canton de Berne, Canton de Zurich, District de Haute-Bavière
- Berne, Munich, Zurich
- Université de Berne
Links toward previous steps (curation, corpus...)
Le document en format XML
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Bornkamm</name><affiliation wicri:level="3"><nlm:affiliation>Institute of Clinical Molecular Biology and Tumor Genetics, Helmholtz Zentrum München, München, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Institute of Clinical Molecular Biology and Tumor Genetics, Helmholtz Zentrum München, München</wicri:regionArea><placeName><region type="land" nuts="1">Bavière</region><region type="district" nuts="2">District de Haute-Bavière</region><settlement type="city">Munich</settlement></placeName></affiliation></author><author><name sortKey="Bachmann, Martin F" sort="Bachmann, Martin F" uniqKey="Bachmann M" first="Martin F" last="Bachmann">Martin F. Bachmann</name><affiliation wicri:level="4"><nlm:affiliation>Department of BioMedical Research, University of Bern, Department of Immunology RIA, University Hospital Bern, Bern, Switzerland.</nlm:affiliation><country xml:lang="fr">Suisse</country><wicri:regionArea>Department of BioMedical Research, University of Bern, Department of Immunology RIA, University Hospital Bern, Bern</wicri:regionArea><placeName><settlement type="city">Berne</settlement><region type="région" nuts="3">Canton de Berne</region></placeName><orgName type="university">Université de Berne</orgName></affiliation></author><author><name sortKey="Kopf, Manfred" sort="Kopf, Manfred" uniqKey="Kopf M" first="Manfred" last="Kopf">Manfred Kopf</name><affiliation wicri:level="3"><nlm:affiliation>Institute of Molecular Health Sciences, ETH Zurich, Zürich, Switzerland.</nlm:affiliation><country xml:lang="fr">Suisse</country><wicri:regionArea>Institute of Molecular Health Sciences, ETH Zurich, Zürich</wicri:regionArea><placeName><settlement type="city">Zurich</settlement><region nuts="3" type="region">Canton de Zurich</region></placeName></affiliation></author></analytic><series><title level="j">European journal of immunology</title><idno type="eISSN">1521-4141</idno><imprint><date when="2019" type="published">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term><term>B-Lymphocytes (cytology)</term><term>B-Lymphocytes (immunology)</term><term>B-Lymphocytes (metabolism)</term><term>Biomarkers (MeSH)</term><term>Cell Differentiation (genetics)</term><term>Cell Differentiation (immunology)</term><term>Cell Proliferation (genetics)</term><term>Germinal Center (immunology)</term><term>Germinal Center (metabolism)</term><term>Glutaredoxins (genetics)</term><term>Glutaredoxins (metabolism)</term><term>Mice (MeSH)</term><term>Mice, Transgenic (MeSH)</term><term>Thioredoxins (genetics)</term><term>Thioredoxins (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term><term>Centre germinatif (immunologie)</term><term>Centre germinatif (métabolisme)</term><term>Différenciation cellulaire (génétique)</term><term>Différenciation cellulaire (immunologie)</term><term>Glutarédoxines (génétique)</term><term>Glutarédoxines (métabolisme)</term><term>Lymphocytes B (cytologie)</term><term>Lymphocytes B (immunologie)</term><term>Lymphocytes B (métabolisme)</term><term>Marqueurs biologiques (MeSH)</term><term>Prolifération cellulaire (génétique)</term><term>Souris (MeSH)</term><term>Souris transgéniques (MeSH)</term><term>Thiorédoxines (génétique)</term><term>Thiorédoxines (métabolisme)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Glutaredoxins</term><term>Thioredoxins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Glutaredoxins</term><term>Thioredoxins</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Biomarkers</term></keywords><keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Lymphocytes B</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>B-Lymphocytes</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Cell Differentiation</term><term>Cell Proliferation</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Différenciation cellulaire</term><term>Glutarédoxines</term><term>Prolifération cellulaire</term><term>Thiorédoxines</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Centre germinatif</term><term>Différenciation cellulaire</term><term>Lymphocytes B</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>B-Lymphocytes</term><term>Cell Differentiation</term><term>Germinal Center</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>B-Lymphocytes</term><term>Germinal Center</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Centre germinatif</term><term>Glutarédoxines</term><term>Lymphocytes B</term><term>Thiorédoxines</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Mice</term><term>Mice, Transgenic</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Marqueurs biologiques</term><term>Souris</term><term>Souris transgéniques</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Antioxidant systems maintain cellular redox homeostasis. The thioredoxin-1 (Trx1) and the glutathione (GSH)/glutaredoxin-1 (Grx1) systems are key players in preserving cytosolic redox balance. In fact, T lymphocytes critically rely on reducing equivalents from the Trx1 system for DNA biosynthesis during metabolic reprogramming upon activation. We here show that the Trx1 system is also indispensable for development and functionality of marginal zone (MZ) B cells and B1 cells in mice. In contrast, development of conventional B cells, follicular B-cell homeostasis, germinal center reactions, and antibody responses are redundantly sustained by both antioxidant pathways. Proliferating B2 cells lacking Txnrd1 have increased glutathione (GSH) levels and upregulated cytosolic Grx1, which is barely detectable in expanding thymocytes. These results suggest that the redox capacity driving proliferation is more robust and flexible in B cells than in T cells, which may have profound implications for the therapy of B and T-cell neoplasms.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">30802940</PMID><DateCompleted><Year>2020</Year><Month>05</Month><Day>26</Day></DateCompleted><DateRevised><Year>2020</Year><Month>05</Month><Day>26</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1521-4141</ISSN><JournalIssue CitedMedium="Internet"><Volume>49</Volume><Issue>5</Issue><PubDate><Year>2019</Year><Month>05</Month></PubDate></JournalIssue><Title>European journal of immunology</Title><ISOAbbreviation>Eur J Immunol</ISOAbbreviation></Journal><ArticleTitle>The thioredoxin-1 and glutathione/glutaredoxin-1 systems redundantly fuel murine B-cell development and responses.</ArticleTitle><Pagination><MedlinePgn>709-723</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/eji.201848044</ELocationID><Abstract><AbstractText>Antioxidant systems maintain cellular redox homeostasis. The thioredoxin-1 (Trx1) and the glutathione (GSH)/glutaredoxin-1 (Grx1) systems are key players in preserving cytosolic redox balance. In fact, T lymphocytes critically rely on reducing equivalents from the Trx1 system for DNA biosynthesis during metabolic reprogramming upon activation. We here show that the Trx1 system is also indispensable for development and functionality of marginal zone (MZ) B cells and B1 cells in mice. In contrast, development of conventional B cells, follicular B-cell homeostasis, germinal center reactions, and antibody responses are redundantly sustained by both antioxidant pathways. Proliferating B2 cells lacking Txnrd1 have increased glutathione (GSH) levels and upregulated cytosolic Grx1, which is barely detectable in expanding thymocytes. These results suggest that the redox capacity driving proliferation is more robust and flexible in B cells than in T cells, which may have profound implications for the therapy of B and T-cell neoplasms.</AbstractText><CopyrightInformation>© 2019 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Muri</LastName><ForeName>Jonathan</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Institute of Molecular Health Sciences, ETH Zurich, Zürich, Switzerland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Thut</LastName><ForeName>Helen</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Institute of Molecular Health Sciences, ETH Zurich, Zürich, Switzerland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Heer</LastName><ForeName>Sebastian</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Institute of Molecular Health Sciences, ETH Zurich, Zürich, Switzerland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Krueger</LastName><ForeName>Caroline C</ForeName><Initials>CC</Initials><AffiliationInfo><Affiliation>Department of BioMedical Research, University of Bern, Department of Immunology RIA, University Hospital Bern, Bern, Switzerland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bornkamm</LastName><ForeName>Georg W</ForeName><Initials>GW</Initials><AffiliationInfo><Affiliation>Institute of Clinical Molecular Biology and Tumor Genetics, Helmholtz Zentrum München, München, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bachmann</LastName><ForeName>Martin F</ForeName><Initials>MF</Initials><AffiliationInfo><Affiliation>Department of BioMedical Research, University of Bern, Department of Immunology RIA, University Hospital Bern, Bern, Switzerland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kopf</LastName><ForeName>Manfred</ForeName><Initials>M</Initials><Identifier Source="ORCID">0000-0002-0628-7140</Identifier><AffiliationInfo><Affiliation>Institute of Molecular Health Sciences, ETH Zurich, Zürich, Switzerland.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2019</Year><Month>03</Month><Day>01</Day></ArticleDate></Article><MedlineJournalInfo><Country>Germany</Country><MedlineTA>Eur J Immunol</MedlineTA><NlmUniqueID>1273201</NlmUniqueID><ISSNLinking>0014-2980</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015415">Biomarkers</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D054477">Glutaredoxins</NameOfSubstance></Chemical><Chemical><RegistryNumber>52500-60-4</RegistryNumber><NameOfSubstance UI="D013879">Thioredoxins</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001402" MajorTopicYN="N">B-Lymphocytes</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015415" MajorTopicYN="N">Biomarkers</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002454" MajorTopicYN="N">Cell Differentiation</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D049109" MajorTopicYN="N">Cell Proliferation</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018858" MajorTopicYN="N">Germinal Center</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D054477" MajorTopicYN="N">Glutaredoxins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008822" MajorTopicYN="N">Mice, Transgenic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013879" MajorTopicYN="N">Thioredoxins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">Antibody responses</Keyword><Keyword MajorTopicYN="Y">B cell development</Keyword><Keyword MajorTopicYN="Y">Glutaredoxin-1</Keyword><Keyword MajorTopicYN="Y">Thioredoxin-1</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2018</Year><Month>12</Month><Day>03</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2019</Year><Month>01</Month><Day>22</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2019</Year><Month>02</Month><Day>22</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2019</Year><Month>2</Month><Day>26</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>5</Month><Day>27</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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Bachmann</name><name sortKey="Heer, Sebastian" sort="Heer, Sebastian" uniqKey="Heer S" first="Sebastian" last="Heer">Sebastian Heer</name><name sortKey="Kopf, Manfred" sort="Kopf, Manfred" uniqKey="Kopf M" first="Manfred" last="Kopf">Manfred Kopf</name><name sortKey="Krueger, Caroline C" sort="Krueger, Caroline C" uniqKey="Krueger C" first="Caroline C" last="Krueger">Caroline C. Krueger</name><name sortKey="Thut, Helen" sort="Thut, Helen" uniqKey="Thut H" first="Helen" last="Thut">Helen Thut</name></country><country name="Allemagne"><region name="Bavière"><name sortKey="Bornkamm, Georg W" sort="Bornkamm, Georg W" uniqKey="Bornkamm G" first="Georg W" last="Bornkamm">Georg W. Bornkamm</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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|clé= pubmed:30802940
|texte= The thioredoxin-1 and glutathione/glutaredoxin-1 systems redundantly fuel murine B-cell development and responses.
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