Sestrin2 Mediates IL-4-induced IgE Class Switching by Enhancing Germline ε Transcription in B Cells.
Identifieur interne : 000048 ( Main/Exploration ); précédent : 000047; suivant : 000049Sestrin2 Mediates IL-4-induced IgE Class Switching by Enhancing Germline ε Transcription in B Cells.
Auteurs : You-Sun Shim [Corée du Sud] ; Solji Lee [Corée du Sud] ; Hwan-Woo Park [Corée du Sud] ; Seok-Rae Park [Corée du Sud]Source :
- Immune network [ 1598-2629 ] ; 2020.
Abstract
Sestrin2 (Sesn2), a metabolic regulator, accumulates in response to a diverse array of cellular stresses. Sesn2 regulates cellular metabolism by inhibiting the mammalian target of rapamycin complex 1 through the AMP-activated protein kinase (AMPK) signaling pathway. Recently, researchers reported that Sesn2 regulates the differentiation and function of innate immune cells and T cells; however, the role of Sesn2 in B cells is largely unknown. In this study, we investigated the role of Sesn2 in Ig class switching and Ig production in mouse B cells. We observed that mouse B cells express Sesn2 mRNA. Interestingly, the expression of germline ε transcripts (GLTε) was selectively decreased in lipopolysaccharide-stimulated Sesn2-/- splenocytes. Overexpression of Sesn2 increased GLTε promoter activity in B cells. In addition, AICAR (an activator of AMPK) selectively increased IL-4-induced GLTε expression and surface IgE (sIgE) expression in splenocytes. Furthermore, AICAR selectively enhanced IL-4-induced GLTε expression, sIgE expression, and IgE production by anti-CD40-stimulated B cells. We observed that ovalbumin (OVA)-specific IgE concentration was reduced in OVA-challenged Sesn2-/- mice. Taken together, these results indicate that Sesn2-AMPK signaling selectively enhances IL-4-induced IgE class switching and IgE production by B cells, suggesting that this could be a therapeutic strategy targeting Sesn2 in IgE-mediated allergic diseases.
DOI: 10.4110/in.2020.20.e19
PubMed: 32395371
PubMed Central: PMC7192835
Affiliations:
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Korea.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Cell Biology, College of Medicine, Konyang University, Daejeon 35365</wicri:regionArea><wicri:noRegion>Daejeon 35365</wicri:noRegion></affiliation></author><author><name sortKey="Park, Hwan Woo" sort="Park, Hwan Woo" uniqKey="Park H" first="Hwan-Woo" last="Park">Hwan-Woo Park</name><affiliation wicri:level="1"><nlm:affiliation>Department of Cell Biology, College of Medicine, Konyang University, Daejeon 35365, Korea.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Cell Biology, College of Medicine, Konyang University, Daejeon 35365</wicri:regionArea><wicri:noRegion>Daejeon 35365</wicri:noRegion></affiliation></author><author><name sortKey="Park, Seok Rae" sort="Park, Seok Rae" uniqKey="Park S" first="Seok-Rae" last="Park">Seok-Rae Park</name><affiliation wicri:level="1"><nlm:affiliation>Department of Microbiology, Myunggok Medical Research Institute, College of Medicine, Konyang University, Daejeon 35365, Korea.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Microbiology, Myunggok Medical Research Institute, College of Medicine, Konyang University, Daejeon 35365</wicri:regionArea><wicri:noRegion>Daejeon 35365</wicri:noRegion></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2020">2020</date><idno type="RBID">pubmed:32395371</idno><idno type="pmid">32395371</idno><idno type="doi">10.4110/in.2020.20.e19</idno><idno type="pmc">PMC7192835</idno><idno type="wicri:Area/Main/Corpus">000076</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000076</idno><idno type="wicri:Area/Main/Curation">000076</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Curation">000076</idno><idno type="wicri:Area/Main/Exploration">000076</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Sestrin2 Mediates IL-4-induced IgE Class Switching by Enhancing Germline ε Transcription in B Cells.</title><author><name sortKey="Shim, You Sun" sort="Shim, You Sun" uniqKey="Shim Y" first="You-Sun" last="Shim">You-Sun Shim</name><affiliation wicri:level="1"><nlm:affiliation>Department of Microbiology, Myunggok Medical Research Institute, College of Medicine, Konyang University, Daejeon 35365, Korea.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Microbiology, Myunggok Medical Research Institute, College of Medicine, Konyang University, Daejeon 35365</wicri:regionArea><wicri:noRegion>Daejeon 35365</wicri:noRegion></affiliation></author><author><name sortKey="Lee, Solji" sort="Lee, Solji" uniqKey="Lee S" first="Solji" last="Lee">Solji Lee</name><affiliation wicri:level="1"><nlm:affiliation>Department of Cell Biology, College of Medicine, Konyang University, Daejeon 35365, Korea.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Cell Biology, College of Medicine, Konyang University, Daejeon 35365</wicri:regionArea><wicri:noRegion>Daejeon 35365</wicri:noRegion></affiliation></author><author><name sortKey="Park, Hwan Woo" sort="Park, Hwan Woo" uniqKey="Park H" first="Hwan-Woo" last="Park">Hwan-Woo Park</name><affiliation wicri:level="1"><nlm:affiliation>Department of Cell Biology, College of Medicine, Konyang University, Daejeon 35365, Korea.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Cell Biology, College of Medicine, Konyang University, Daejeon 35365</wicri:regionArea><wicri:noRegion>Daejeon 35365</wicri:noRegion></affiliation></author><author><name sortKey="Park, Seok Rae" sort="Park, Seok Rae" uniqKey="Park S" first="Seok-Rae" last="Park">Seok-Rae Park</name><affiliation wicri:level="1"><nlm:affiliation>Department of Microbiology, Myunggok Medical Research Institute, College of Medicine, Konyang University, Daejeon 35365, Korea.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Microbiology, Myunggok Medical Research Institute, College of Medicine, Konyang University, Daejeon 35365</wicri:regionArea><wicri:noRegion>Daejeon 35365</wicri:noRegion></affiliation></author></analytic><series><title level="j">Immune network</title><idno type="ISSN">1598-2629</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">Sestrin2 (Sesn2), a metabolic regulator, accumulates in response to a diverse array of cellular stresses. Sesn2 regulates cellular metabolism by inhibiting the mammalian target of rapamycin complex 1 through the AMP-activated protein kinase (AMPK) signaling pathway. Recently, researchers reported that Sesn2 regulates the differentiation and function of innate immune cells and T cells; however, the role of Sesn2 in B cells is largely unknown. In this study, we investigated the role of Sesn2 in Ig class switching and Ig production in mouse B cells. We observed that mouse B cells express Sesn2 mRNA. Interestingly, the expression of germline ε transcripts (GLTε) was selectively decreased in lipopolysaccharide-stimulated <i>Sesn2</i><sup>-/-</sup> splenocytes. Overexpression of Sesn2 increased GLTε promoter activity in B cells. In addition, AICAR (an activator of AMPK) selectively increased IL-4-induced GLTε expression and surface IgE (sIgE) expression in splenocytes. Furthermore, AICAR selectively enhanced IL-4-induced GLTε expression, sIgE expression, and IgE production by anti-CD40-stimulated B cells. We observed that ovalbumin (OVA)-specific IgE concentration was reduced in OVA-challenged <i>Sesn2</i><sup>-/-</sup> mice. Taken together, these results indicate that Sesn2-AMPK signaling selectively enhances IL-4-induced IgE class switching and IgE production by B cells, suggesting that this could be a therapeutic strategy targeting Sesn2 in IgE-mediated allergic diseases.</div></front></TEI><pubmed><MedlineCitation Status="PubMed-not-MEDLINE" Owner="NLM"><PMID Version="1">32395371</PMID><DateRevised><Year>2020</Year><Month>09</Month><Day>28</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Print">1598-2629</ISSN><JournalIssue CitedMedium="Print"><Volume>20</Volume><Issue>2</Issue><PubDate><Year>2020</Year><Month>Apr</Month></PubDate></JournalIssue><Title>Immune network</Title><ISOAbbreviation>Immune Netw</ISOAbbreviation></Journal><ArticleTitle>Sestrin2 Mediates IL-4-induced IgE Class Switching by Enhancing Germline ε Transcription in B Cells.</ArticleTitle><Pagination><MedlinePgn>e19</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.4110/in.2020.20.e19</ELocationID><Abstract><AbstractText>Sestrin2 (Sesn2), a metabolic regulator, accumulates in response to a diverse array of cellular stresses. Sesn2 regulates cellular metabolism by inhibiting the mammalian target of rapamycin complex 1 through the AMP-activated protein kinase (AMPK) signaling pathway. Recently, researchers reported that Sesn2 regulates the differentiation and function of innate immune cells and T cells; however, the role of Sesn2 in B cells is largely unknown. In this study, we investigated the role of Sesn2 in Ig class switching and Ig production in mouse B cells. We observed that mouse B cells express Sesn2 mRNA. Interestingly, the expression of germline ε transcripts (GLTε) was selectively decreased in lipopolysaccharide-stimulated <i>Sesn2</i><sup>-/-</sup> splenocytes. Overexpression of Sesn2 increased GLTε promoter activity in B cells. In addition, AICAR (an activator of AMPK) selectively increased IL-4-induced GLTε expression and surface IgE (sIgE) expression in splenocytes. Furthermore, AICAR selectively enhanced IL-4-induced GLTε expression, sIgE expression, and IgE production by anti-CD40-stimulated B cells. We observed that ovalbumin (OVA)-specific IgE concentration was reduced in OVA-challenged <i>Sesn2</i><sup>-/-</sup> mice. Taken together, these results indicate that Sesn2-AMPK signaling selectively enhances IL-4-induced IgE class switching and IgE production by B cells, suggesting that this could be a therapeutic strategy targeting Sesn2 in IgE-mediated allergic diseases.</AbstractText><CopyrightInformation>Copyright © 2020. The Korean Association of Immunologists.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Shim</LastName><ForeName>You-Sun</ForeName><Initials>YS</Initials><AffiliationInfo><Affiliation>Department of Microbiology, Myunggok Medical Research Institute, College of Medicine, Konyang University, Daejeon 35365, Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Solji</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Cell Biology, College of Medicine, Konyang University, Daejeon 35365, Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Park</LastName><ForeName>Hwan-Woo</ForeName><Initials>HW</Initials><Identifier Source="ORCID">https://orcid.org/0000-0001-8029-2004</Identifier><AffiliationInfo><Affiliation>Department of Cell Biology, College of Medicine, Konyang University, Daejeon 35365, Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Park</LastName><ForeName>Seok-Rae</ForeName><Initials>SR</Initials><Identifier Source="ORCID">https://orcid.org/0000-0002-1407-4495</Identifier><AffiliationInfo><Affiliation>Department of Microbiology, Myunggok Medical Research Institute, College of Medicine, Konyang University, Daejeon 35365, Korea.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2020</Year><Month>01</Month><Day>20</Day></ArticleDate></Article><MedlineJournalInfo><Country>Korea (South)</Country><MedlineTA>Immune Netw</MedlineTA><NlmUniqueID>101137270</NlmUniqueID><ISSNLinking>1598-2629</ISSNLinking></MedlineJournalInfo><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">AMPK</Keyword><Keyword MajorTopicYN="N">B cells</Keyword><Keyword MajorTopicYN="N">Germline ε transcripts</Keyword><Keyword MajorTopicYN="N">IgE</Keyword><Keyword MajorTopicYN="N">Sesn2</Keyword></KeywordList><CoiStatement>Conflict of Interest: The author declares no potential conflicts of interest.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2019</Year><Month>09</Month><Day>22</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2019</Year><Month>12</Month><Day>23</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2019</Year><Month>12</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2020</Year><Month>5</Month><Day>13</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2020</Year><Month>5</Month><Day>13</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>5</Month><Day>13</Day><Hour>6</Hour><Minute>1</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId 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