Interferon-λ Enhances the Differentiation of Naive B Cells into Plasmablasts via the mTORC1 Pathway.
Identifieur interne : 000101 ( Main/Exploration ); précédent : 000100; suivant : 000102Interferon-λ Enhances the Differentiation of Naive B Cells into Plasmablasts via the mTORC1 Pathway.
Auteurs : Mohammedyaseen Syedbasha [Suisse] ; Ferdinando Bonfiglio [Suisse] ; Janina Linnik [Suisse] ; Claudia Stuehler [Suisse] ; Daniel Wüthrich [Suisse] ; Adrian Egli [Suisse]Source :
- Cell reports [ 2211-1247 ] ; 2020.
Abstract
Type III interferon (interferon lambda [IFN-λ]) is known to be a potential immune modulator, but the mechanisms behind its immune-modulatory functions and its impact on plasmablast differentiation in humans remain unknown. Human B cells and their subtypes directly respond to IFN-λ. Using B cell transcriptome profiling, we investigate the immune-modulatory role of IFN-λ in B cells. We find that IFN-λ-induced gene expression in B cells is steady, prolonged, and importantly, cell type specific. Furthermore, IFN-λ enhances the mTORC1 (mammalian/mechanistic target of rapamycin complex 1) pathway in B cells activated by the B cell receptor (BCR/anti-IgM). Engagement of mTORC1 by BCR and IFN-λ induces cell-cycle progress in B cells. Subsequently, IFN-λ boosts the differentiation of naive B cells into plasmablasts upon activation, and the cells gain effector functions such as cytokine release (IL-6 and IL-10) and antibody production. Our study shows how IFN-λ systematically boosts the differentiation of naive B cells into plasmablasts by enhancing the mTORC1 pathway and cell-cycle progression in activated B cells.
DOI: 10.1016/j.celrep.2020.108211
PubMed: 33027651
Affiliations:
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Electronic address: m.syedbasha@unibas.ch.</nlm:affiliation><country xml:lang="fr">Suisse</country><wicri:regionArea>Applied Microbiology Research, Department of Biomedicine, University of Basel, Basel</wicri:regionArea><wicri:noRegion>Basel</wicri:noRegion></affiliation></author><author><name sortKey="Bonfiglio, Ferdinando" sort="Bonfiglio, Ferdinando" uniqKey="Bonfiglio F" first="Ferdinando" last="Bonfiglio">Ferdinando Bonfiglio</name><affiliation wicri:level="1"><nlm:affiliation>Applied Microbiology Research, Department of Biomedicine, University of Basel, Basel, Switzerland; Swiss Institute for Bioinformatics, Basel, Switzerland.</nlm:affiliation><country xml:lang="fr">Suisse</country><wicri:regionArea>Applied Microbiology Research, Department of Biomedicine, University of Basel, Basel, Switzerland; Swiss Institute for Bioinformatics, Basel</wicri:regionArea><wicri:noRegion>Basel</wicri:noRegion></affiliation></author><author><name sortKey="Linnik, Janina" sort="Linnik, Janina" uniqKey="Linnik J" first="Janina" last="Linnik">Janina Linnik</name><affiliation wicri:level="1"><nlm:affiliation>Swiss Institute for Bioinformatics, Basel, Switzerland; Department of Biosystems Science and Engineering, ETH Zurich, Basel, Switzerland.</nlm:affiliation><country xml:lang="fr">Suisse</country><wicri:regionArea>Swiss Institute for Bioinformatics, Basel, Switzerland; Department of Biosystems Science and Engineering, ETH Zurich, Basel</wicri:regionArea><wicri:noRegion>Basel</wicri:noRegion></affiliation></author><author><name sortKey="Stuehler, Claudia" sort="Stuehler, Claudia" uniqKey="Stuehler C" first="Claudia" last="Stuehler">Claudia Stuehler</name><affiliation wicri:level="1"><nlm:affiliation>Infection Biology Laboratory, Department of Biomedicine, University of Basel, Basel, Switzerland.</nlm:affiliation><country xml:lang="fr">Suisse</country><wicri:regionArea>Infection Biology Laboratory, Department of Biomedicine, University of Basel, Basel</wicri:regionArea><wicri:noRegion>Basel</wicri:noRegion></affiliation></author><author><name sortKey="Wuthrich, Daniel" sort="Wuthrich, Daniel" uniqKey="Wuthrich D" first="Daniel" last="Wüthrich">Daniel Wüthrich</name><affiliation wicri:level="1"><nlm:affiliation>Applied Microbiology Research, Department of Biomedicine, University of Basel, Basel, Switzerland; Swiss Institute for Bioinformatics, Basel, Switzerland; Clinical Bacteriology and Mycology, University Hospital Basel, Basel, Switzerland.</nlm:affiliation><country xml:lang="fr">Suisse</country><wicri:regionArea>Applied Microbiology Research, Department of Biomedicine, University of Basel, Basel, Switzerland; Swiss Institute for Bioinformatics, Basel, Switzerland; Clinical Bacteriology and Mycology, University Hospital Basel, Basel</wicri:regionArea><wicri:noRegion>Basel</wicri:noRegion></affiliation></author><author><name sortKey="Egli, Adrian" sort="Egli, Adrian" uniqKey="Egli A" first="Adrian" last="Egli">Adrian Egli</name><affiliation wicri:level="1"><nlm:affiliation>Applied Microbiology Research, Department of Biomedicine, University of Basel, Basel, Switzerland; Clinical Bacteriology and Mycology, University Hospital Basel, Basel, Switzerland. Electronic address: adrian.egli@usb.ch.</nlm:affiliation><country xml:lang="fr">Suisse</country><wicri:regionArea>Applied Microbiology Research, Department of Biomedicine, University of Basel, Basel, Switzerland; Clinical Bacteriology and Mycology, University Hospital Basel, Basel</wicri:regionArea><wicri:noRegion>Basel</wicri:noRegion></affiliation></author></analytic><series><title level="j">Cell reports</title><idno type="eISSN">2211-1247</idno><imprint><date when="2020" type="published">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Type III interferon (interferon lambda [IFN-λ]) is known to be a potential immune modulator, but the mechanisms behind its immune-modulatory functions and its impact on plasmablast differentiation in humans remain unknown. Human B cells and their subtypes directly respond to IFN-λ. Using B cell transcriptome profiling, we investigate the immune-modulatory role of IFN-λ in B cells. We find that IFN-λ-induced gene expression in B cells is steady, prolonged, and importantly, cell type specific. Furthermore, IFN-λ enhances the mTORC1 (mammalian/mechanistic target of rapamycin complex 1) pathway in B cells activated by the B cell receptor (BCR/anti-IgM). Engagement of mTORC1 by BCR and IFN-λ induces cell-cycle progress in B cells. Subsequently, IFN-λ boosts the differentiation of naive B cells into plasmablasts upon activation, and the cells gain effector functions such as cytokine release (IL-6 and IL-10) and antibody production. Our study shows how IFN-λ systematically boosts the differentiation of naive B cells into plasmablasts by enhancing the mTORC1 pathway and cell-cycle progression in activated B cells.</div></front></TEI><pubmed><MedlineCitation Status="In-Data-Review" Owner="NLM"><PMID Version="1">33027651</PMID><DateRevised><Year>2020</Year><Month>10</Month><Day>07</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">2211-1247</ISSN><JournalIssue CitedMedium="Internet"><Volume>33</Volume><Issue>1</Issue><PubDate><Year>2020</Year><Month>Oct</Month><Day>06</Day></PubDate></JournalIssue><Title>Cell reports</Title><ISOAbbreviation>Cell Rep</ISOAbbreviation></Journal><ArticleTitle>Interferon-λ Enhances the Differentiation of Naive B Cells into Plasmablasts via the mTORC1 Pathway.</ArticleTitle><Pagination><MedlinePgn>108211</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S2211-1247(20)31200-6</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.celrep.2020.108211</ELocationID><Abstract><AbstractText>Type III interferon (interferon lambda [IFN-λ]) is known to be a potential immune modulator, but the mechanisms behind its immune-modulatory functions and its impact on plasmablast differentiation in humans remain unknown. Human B cells and their subtypes directly respond to IFN-λ. Using B cell transcriptome profiling, we investigate the immune-modulatory role of IFN-λ in B cells. We find that IFN-λ-induced gene expression in B cells is steady, prolonged, and importantly, cell type specific. Furthermore, IFN-λ enhances the mTORC1 (mammalian/mechanistic target of rapamycin complex 1) pathway in B cells activated by the B cell receptor (BCR/anti-IgM). Engagement of mTORC1 by BCR and IFN-λ induces cell-cycle progress in B cells. Subsequently, IFN-λ boosts the differentiation of naive B cells into plasmablasts upon activation, and the cells gain effector functions such as cytokine release (IL-6 and IL-10) and antibody production. Our study shows how IFN-λ systematically boosts the differentiation of naive B cells into plasmablasts by enhancing the mTORC1 pathway and cell-cycle progression in activated B cells.</AbstractText><CopyrightInformation>Copyright © 2020 The Author(s). Published by Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Syedbasha</LastName><ForeName>Mohammedyaseen</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Applied Microbiology Research, Department of Biomedicine, University of Basel, Basel, Switzerland. Electronic address: m.syedbasha@unibas.ch.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bonfiglio</LastName><ForeName>Ferdinando</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Applied Microbiology Research, Department of Biomedicine, University of Basel, Basel, Switzerland; Swiss Institute for Bioinformatics, Basel, Switzerland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Linnik</LastName><ForeName>Janina</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Swiss Institute for Bioinformatics, Basel, Switzerland; Department of Biosystems Science and Engineering, ETH Zurich, Basel, Switzerland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Stuehler</LastName><ForeName>Claudia</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Infection Biology Laboratory, Department of Biomedicine, University of Basel, Basel, Switzerland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wüthrich</LastName><ForeName>Daniel</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Applied Microbiology Research, Department of Biomedicine, University of Basel, Basel, Switzerland; Swiss Institute for Bioinformatics, Basel, Switzerland; Clinical Bacteriology and Mycology, University Hospital Basel, Basel, Switzerland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Egli</LastName><ForeName>Adrian</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Applied Microbiology Research, Department of Biomedicine, University of Basel, Basel, Switzerland; Clinical Bacteriology and Mycology, University Hospital Basel, Basel, Switzerland. Electronic address: adrian.egli@usb.ch.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Cell Rep</MedlineTA><NlmUniqueID>101573691</NlmUniqueID></MedlineJournalInfo><CitationSubset>IM</CitationSubset><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">B cell activation</Keyword><Keyword MajorTopicYN="N">JAK-STAT signaling</Keyword><Keyword MajorTopicYN="N">cell cycle</Keyword><Keyword MajorTopicYN="N">effector function</Keyword><Keyword MajorTopicYN="N">immune modulation</Keyword><Keyword MajorTopicYN="N">interferon lambda</Keyword><Keyword MajorTopicYN="N">mTORC1 pathway</Keyword><Keyword MajorTopicYN="N">phosphorylation</Keyword><Keyword MajorTopicYN="N">plasmablast differentiation</Keyword><Keyword MajorTopicYN="N">transcriptomics</Keyword></KeywordList><CoiStatement>Declaration of Interests The authors declare no competing interests.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2019</Year><Month>10</Month><Day>17</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2020</Year><Month>06</Month><Day>24</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2020</Year><Month>09</Month><Day>09</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2020</Year><Month>10</Month><Day>7</Day><Hour>20</Hour><Minute>5</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2020</Year><Month>10</Month><Day>8</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>10</Month><Day>8</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">33027651</ArticleId><ArticleId IdType="pii">S2211-1247(20)31200-6</ArticleId><ArticleId IdType="doi">10.1016/j.celrep.2020.108211</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Suisse</li></country></list><tree><country name="Suisse"><noRegion><name sortKey="Syedbasha, Mohammedyaseen" sort="Syedbasha, Mohammedyaseen" uniqKey="Syedbasha M" first="Mohammedyaseen" last="Syedbasha">Mohammedyaseen Syedbasha</name></noRegion><name sortKey="Bonfiglio, Ferdinando" sort="Bonfiglio, Ferdinando" uniqKey="Bonfiglio F" first="Ferdinando" last="Bonfiglio">Ferdinando Bonfiglio</name><name sortKey="Egli, Adrian" sort="Egli, Adrian" uniqKey="Egli A" first="Adrian" last="Egli">Adrian Egli</name><name sortKey="Linnik, Janina" sort="Linnik, Janina" uniqKey="Linnik J" first="Janina" last="Linnik">Janina Linnik</name><name sortKey="Stuehler, Claudia" sort="Stuehler, Claudia" uniqKey="Stuehler C" first="Claudia" last="Stuehler">Claudia Stuehler</name><name sortKey="Wuthrich, Daniel" sort="Wuthrich, Daniel" uniqKey="Wuthrich D" first="Daniel" last="Wüthrich">Daniel Wüthrich</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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