T-cell-specific mTOR deletion in mice ameliorated CD4+ T-cell survival in lethal sepsis induced by severe invasive candidiasis.
Identifieur interne : 000222 ( Main/Exploration ); précédent : 000221; suivant : 000223T-cell-specific mTOR deletion in mice ameliorated CD4+ T-cell survival in lethal sepsis induced by severe invasive candidiasis.
Auteurs : Hao Wang [République populaire de Chine] ; Guangxu Bai [République populaire de Chine] ; Na Cui [République populaire de Chine] ; Wen Han [République populaire de Chine] ; Yun Long [République populaire de Chine]Source :
- Virulence [ 2150-5608 ] ; 2019.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Apoptose (MeSH), Autophagie (MeSH), Candidose (immunologie), Complexe de la sclérose tubéreuse (génétique), Délétion de gène (MeSH), Lymphocytes T CD4+ (anatomopathologie), Lymphocytes T CD4+ (immunologie), Mâle (MeSH), Sepsie (immunologie), Sepsie (microbiologie), Souris (MeSH), Souris knockout (MeSH), Survie cellulaire (immunologie), Sérine-thréonine kinases TOR (génétique), Sérine-thréonine kinases TOR (immunologie), Transduction du signal (MeSH).
- MESH :
- anatomopathologie : Lymphocytes T CD4+.
- génétique : Complexe de la sclérose tubéreuse, Sérine-thréonine kinases TOR.
- immunologie : Candidose, Lymphocytes T CD4+, Sepsie, Survie cellulaire, Sérine-thréonine kinases TOR.
- microbiologie : Sepsie.
- Animaux, Apoptose, Autophagie, Délétion de gène, Mâle, Souris, Souris knockout, Transduction du signal.
English descriptors
- KwdEn :
- Animals (MeSH), Apoptosis (MeSH), Autophagy (MeSH), CD4-Positive T-Lymphocytes (immunology), CD4-Positive T-Lymphocytes (pathology), Candidiasis (immunology), Cell Survival (immunology), Gene Deletion (MeSH), Male (MeSH), Mice (MeSH), Mice, Knockout (MeSH), Sepsis (immunology), Sepsis (microbiology), Signal Transduction (MeSH), TOR Serine-Threonine Kinases (genetics), TOR Serine-Threonine Kinases (immunology), Tuberous Sclerosis (genetics).
- MESH :
- chemical , genetics : TOR Serine-Threonine Kinases.
- genetics : Tuberous Sclerosis.
- immunology : CD4-Positive T-Lymphocytes, Candidiasis, Cell Survival, Sepsis, TOR Serine-Threonine Kinases.
- microbiology : Sepsis.
- pathology : CD4-Positive T-Lymphocytes.
- Animals, Apoptosis, Autophagy, Gene Deletion, Male, Mice, Mice, Knockout, Signal Transduction.
Abstract
The mammalian target of rapamycin (mTOR) pathway can mediate T-cell survival; however, the role of this pathway in T-cell survival during fungal sepsis is unclear. Here, we investigated the role of the mTOR pathway in CD4+ T-cell survival in a mouse model of rapidly progressive lethal sepsis induced by severe invasive candidiasis and explored the possible mechanism. The decrease in CD4+ T-cell survival following fungal sepsis was ameliorated in mice with a T-cell-specific mTOR deletion, whereas it was exacerbated in mice with a T-cell-specific tuberous sclerosis complex (TSC)1 deletion. To explore the mechanism further, we measured expression of autophagy proteins light chain 3B and p62/sequestosome 1 in CD4+ T cells. Both proteins were increased in T-cell-specific mTOR knockout mice but lower in T-cell-specific TSC1 knockout mice. Transmission electron microscopy revealed that T-cell-specific mTOR knockout mice had more autophagosomes than wild-type mice following fungal sepsis. CD4+ T-cell mTOR knockout decreased CD4+ T-cell apoptosis in fungal sepsis. Most notably, the T-cell-specific mTOR deletion mice had an increased survival rate after fungal sepsis. These results suggest that the mTOR pathway plays a vital role in CD4+ T-cell survival during fungal sepsis, partly through the autophagy-apoptosis pathway.
DOI: 10.1080/21505594.2019.1685151
PubMed: 31668132
PubMed Central: PMC6844314
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">T-cell-specific mTOR deletion in mice ameliorated CD4<sup>+</sup> T-cell survival in lethal sepsis induced by severe invasive candidiasis.</title><author><name sortKey="Wang, Hao" sort="Wang, Hao" uniqKey="Wang H" first="Hao" last="Wang">Hao Wang</name><affiliation wicri:level="3"><nlm:affiliation>Department of Critical Care Medicine, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Science, Beijing, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Critical Care Medicine, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Science, Beijing</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author><author><name sortKey="Bai, Guangxu" sort="Bai, Guangxu" uniqKey="Bai G" first="Guangxu" last="Bai">Guangxu Bai</name><affiliation wicri:level="3"><nlm:affiliation>Department of Critical Care Medicine, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Science, Beijing, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Critical Care Medicine, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Science, Beijing</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author><author><name sortKey="Cui, Na" sort="Cui, Na" uniqKey="Cui N" first="Na" last="Cui">Na Cui</name><affiliation wicri:level="3"><nlm:affiliation>Department of Critical Care Medicine, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Science, Beijing, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Critical Care Medicine, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Science, Beijing</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation><affiliation wicri:level="3"><nlm:affiliation>Department of Clinical Laboratory, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Science; Beijing Key Laboratory for Mechanisms Research and Precision Diagnosis of Invasive Fungal Diseases, Beijing, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Clinical Laboratory, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Science; Beijing Key Laboratory for Mechanisms Research and Precision Diagnosis of Invasive Fungal Diseases, Beijing</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author><author><name sortKey="Han, Wen" sort="Han, Wen" uniqKey="Han W" first="Wen" last="Han">Wen Han</name><affiliation wicri:level="3"><nlm:affiliation>Department of Critical Care Medicine, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Science, Beijing, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Critical Care Medicine, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Science, Beijing</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author><author><name sortKey="Long, Yun" sort="Long, Yun" uniqKey="Long Y" first="Yun" last="Long">Yun Long</name><affiliation wicri:level="3"><nlm:affiliation>Department of Critical Care Medicine, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Science, Beijing, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Critical Care Medicine, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Science, Beijing</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2019">2019</date><idno type="RBID">pubmed:31668132</idno><idno type="pmid">31668132</idno><idno type="doi">10.1080/21505594.2019.1685151</idno><idno type="pmc">PMC6844314</idno><idno type="wicri:Area/Main/Corpus">000164</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000164</idno><idno type="wicri:Area/Main/Curation">000164</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Curation">000164</idno><idno type="wicri:Area/Main/Exploration">000164</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">T-cell-specific mTOR deletion in mice ameliorated CD4<sup>+</sup> T-cell survival in lethal sepsis induced by severe invasive candidiasis.</title><author><name sortKey="Wang, Hao" sort="Wang, Hao" uniqKey="Wang H" first="Hao" last="Wang">Hao Wang</name><affiliation wicri:level="3"><nlm:affiliation>Department of Critical Care Medicine, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Science, Beijing, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Critical Care Medicine, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Science, Beijing</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author><author><name sortKey="Bai, Guangxu" sort="Bai, Guangxu" uniqKey="Bai G" first="Guangxu" last="Bai">Guangxu Bai</name><affiliation wicri:level="3"><nlm:affiliation>Department of Critical Care Medicine, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Science, Beijing, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Critical Care Medicine, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Science, Beijing</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author><author><name sortKey="Cui, Na" sort="Cui, Na" uniqKey="Cui N" first="Na" last="Cui">Na Cui</name><affiliation wicri:level="3"><nlm:affiliation>Department of Critical Care Medicine, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Science, Beijing, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Critical Care Medicine, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Science, Beijing</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation><affiliation wicri:level="3"><nlm:affiliation>Department of Clinical Laboratory, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Science; Beijing Key Laboratory for Mechanisms Research and Precision Diagnosis of Invasive Fungal Diseases, Beijing, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Clinical Laboratory, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Science; Beijing Key Laboratory for Mechanisms Research and Precision Diagnosis of Invasive Fungal Diseases, Beijing</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author><author><name sortKey="Han, Wen" sort="Han, Wen" uniqKey="Han W" first="Wen" last="Han">Wen Han</name><affiliation wicri:level="3"><nlm:affiliation>Department of Critical Care Medicine, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Science, Beijing, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Critical Care Medicine, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Science, Beijing</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author><author><name sortKey="Long, Yun" sort="Long, Yun" uniqKey="Long Y" first="Yun" last="Long">Yun Long</name><affiliation wicri:level="3"><nlm:affiliation>Department of Critical Care Medicine, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Science, Beijing, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Critical Care Medicine, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Science, Beijing</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author></analytic><series><title level="j">Virulence</title><idno type="eISSN">2150-5608</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>Apoptosis (MeSH)</term><term>Autophagy (MeSH)</term><term>CD4-Positive T-Lymphocytes (immunology)</term><term>CD4-Positive T-Lymphocytes (pathology)</term><term>Candidiasis (immunology)</term><term>Cell Survival (immunology)</term><term>Gene Deletion (MeSH)</term><term>Male (MeSH)</term><term>Mice (MeSH)</term><term>Mice, Knockout (MeSH)</term><term>Sepsis (immunology)</term><term>Sepsis (microbiology)</term><term>Signal Transduction (MeSH)</term><term>TOR Serine-Threonine Kinases (genetics)</term><term>TOR Serine-Threonine Kinases (immunology)</term><term>Tuberous Sclerosis (genetics)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term><term>Apoptose (MeSH)</term><term>Autophagie (MeSH)</term><term>Candidose (immunologie)</term><term>Complexe de la sclérose tubéreuse (génétique)</term><term>Délétion de gène (MeSH)</term><term>Lymphocytes T CD4+ (anatomopathologie)</term><term>Lymphocytes T CD4+ (immunologie)</term><term>Mâle (MeSH)</term><term>Sepsie (immunologie)</term><term>Sepsie (microbiologie)</term><term>Souris (MeSH)</term><term>Souris knockout (MeSH)</term><term>Survie cellulaire (immunologie)</term><term>Sérine-thréonine kinases TOR (génétique)</term><term>Sérine-thréonine kinases TOR (immunologie)</term><term>Transduction du signal (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>TOR Serine-Threonine Kinases</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Lymphocytes T CD4+</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Tuberous Sclerosis</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Complexe de la sclérose tubéreuse</term><term>Sérine-thréonine kinases TOR</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Candidose</term><term>Lymphocytes T CD4+</term><term>Sepsie</term><term>Survie cellulaire</term><term>Sérine-thréonine kinases TOR</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>CD4-Positive T-Lymphocytes</term><term>Candidiasis</term><term>Cell Survival</term><term>Sepsis</term><term>TOR Serine-Threonine Kinases</term></keywords><keywords scheme="MESH" qualifier="microbiologie" xml:lang="fr"><term>Sepsie</term></keywords><keywords scheme="MESH" qualifier="microbiology" xml:lang="en"><term>Sepsis</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>CD4-Positive T-Lymphocytes</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Apoptosis</term><term>Autophagy</term><term>Gene Deletion</term><term>Male</term><term>Mice</term><term>Mice, Knockout</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Apoptose</term><term>Autophagie</term><term>Délétion de gène</term><term>Mâle</term><term>Souris</term><term>Souris knockout</term><term>Transduction du signal</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The mammalian target of rapamycin (mTOR) pathway can mediate T-cell survival; however, the role of this pathway in T-cell survival during fungal sepsis is unclear. Here, we investigated the role of the mTOR pathway in CD4<sup>+</sup> T-cell survival in a mouse model of rapidly progressive lethal sepsis induced by severe invasive candidiasis and explored the possible mechanism. The decrease in CD4<sup>+</sup> T-cell survival following fungal sepsis was ameliorated in mice with a T-cell-specific mTOR deletion, whereas it was exacerbated in mice with a T-cell-specific tuberous sclerosis complex (TSC)1 deletion. To explore the mechanism further, we measured expression of autophagy proteins light chain 3B and p62/sequestosome 1 in CD4<sup>+</sup> T cells. Both proteins were increased in T-cell-specific mTOR knockout mice but lower in T-cell-specific TSC1 knockout mice. Transmission electron microscopy revealed that T-cell-specific mTOR knockout mice had more autophagosomes than wild-type mice following fungal sepsis. CD4<sup>+</sup> T-cell mTOR knockout decreased CD4<sup>+</sup> T-cell apoptosis in fungal sepsis. Most notably, the T-cell-specific mTOR deletion mice had an increased survival rate after fungal sepsis. These results suggest that the mTOR pathway plays a vital role in CD4<sup>+</sup> T-cell survival during fungal sepsis, partly through the autophagy-apoptosis pathway.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">31668132</PMID><DateCompleted><Year>2020</Year><Month>08</Month><Day>03</Day></DateCompleted><DateRevised><Year>2020</Year><Month>08</Month><Day>03</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">2150-5608</ISSN><JournalIssue CitedMedium="Internet"><Volume>10</Volume><Issue>1</Issue><PubDate><Year>2019</Year><Month>12</Month></PubDate></JournalIssue><Title>Virulence</Title><ISOAbbreviation>Virulence</ISOAbbreviation></Journal><ArticleTitle>T-cell-specific mTOR deletion in mice ameliorated CD4<sup>+</sup> T-cell survival in lethal sepsis induced by severe invasive candidiasis.</ArticleTitle><Pagination><MedlinePgn>892-901</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1080/21505594.2019.1685151</ELocationID><Abstract><AbstractText>The mammalian target of rapamycin (mTOR) pathway can mediate T-cell survival; however, the role of this pathway in T-cell survival during fungal sepsis is unclear. Here, we investigated the role of the mTOR pathway in CD4<sup>+</sup> T-cell survival in a mouse model of rapidly progressive lethal sepsis induced by severe invasive candidiasis and explored the possible mechanism. The decrease in CD4<sup>+</sup> T-cell survival following fungal sepsis was ameliorated in mice with a T-cell-specific mTOR deletion, whereas it was exacerbated in mice with a T-cell-specific tuberous sclerosis complex (TSC)1 deletion. To explore the mechanism further, we measured expression of autophagy proteins light chain 3B and p62/sequestosome 1 in CD4<sup>+</sup> T cells. Both proteins were increased in T-cell-specific mTOR knockout mice but lower in T-cell-specific TSC1 knockout mice. Transmission electron microscopy revealed that T-cell-specific mTOR knockout mice had more autophagosomes than wild-type mice following fungal sepsis. CD4<sup>+</sup> T-cell mTOR knockout decreased CD4<sup>+</sup> T-cell apoptosis in fungal sepsis. Most notably, the T-cell-specific mTOR deletion mice had an increased survival rate after fungal sepsis. These results suggest that the mTOR pathway plays a vital role in CD4<sup>+</sup> T-cell survival during fungal sepsis, partly through the autophagy-apoptosis pathway.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Hao</ForeName><Initials>H</Initials><Identifier Source="ORCID">0000-0001-7776-0882</Identifier><AffiliationInfo><Affiliation>Department of Critical Care Medicine, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Science, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bai</LastName><ForeName>Guangxu</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Department of Critical Care Medicine, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Science, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cui</LastName><ForeName>Na</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Department of Critical Care Medicine, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Science, Beijing, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Clinical Laboratory, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Science; Beijing Key Laboratory for Mechanisms Research and Precision Diagnosis of Invasive Fungal Diseases, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Han</LastName><ForeName>Wen</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>Department of Critical Care Medicine, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Science, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Long</LastName><ForeName>Yun</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Critical Care Medicine, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Science, Beijing, China.</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></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Virulence</MedlineTA><NlmUniqueID>101531386</NlmUniqueID><ISSNLinking>2150-5594</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>EC 2.7.1.1</RegistryNumber><NameOfSubstance UI="D058570">TOR Serine-Threonine Kinases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.1.1</RegistryNumber><NameOfSubstance UI="C546843">mTOR protein, mouse</NameOfSubstance></Chemical></ChemicalList><SupplMeshList><SupplMeshName Type="Disease" UI="C536777">Systemic candidiasis</SupplMeshName><SupplMeshName Type="Disease" UI="C565346">Tuberous Sclerosis 1</SupplMeshName></SupplMeshList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017209" MajorTopicYN="Y">Apoptosis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001343" MajorTopicYN="N">Autophagy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015496" MajorTopicYN="N">CD4-Positive T-Lymphocytes</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002177" MajorTopicYN="N">Candidiasis</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002470" MajorTopicYN="N">Cell Survival</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017353" MajorTopicYN="N">Gene Deletion</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018345" MajorTopicYN="N">Mice, Knockout</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018805" MajorTopicYN="N">Sepsis</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000382" MajorTopicYN="Y">microbiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D058570" MajorTopicYN="N">TOR Serine-Threonine Kinases</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014402" MajorTopicYN="N">Tuberous Sclerosis</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">CD4+ T cells</Keyword><Keyword MajorTopicYN="Y">Lethal fungal sepsis</Keyword><Keyword MajorTopicYN="Y">autophagy</Keyword><Keyword MajorTopicYN="Y">mammalian target of rapamycin</Keyword><Keyword MajorTopicYN="Y">severe invasive candidiasis</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2019</Year><Month>11</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2019</Year><Month>11</Month><Day>2</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>8</Month><Day>4</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">31668132</ArticleId><ArticleId IdType="doi">10.1080/21505594.2019.1685151</ArticleId><ArticleId IdType="pmc">PMC6844314</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Mycopathologia. 2016 Aug;181(7-8):485-95</Citation><ArticleIdList><ArticleId IdType="pubmed">26994763</ArticleId></ArticleIdList></Reference><Reference><Citation>BMB Rep. 2016 Aug;49(8):424-30</Citation><ArticleIdList><ArticleId IdType="pubmed">27418283</ArticleId></ArticleIdList></Reference><Reference><Citation>Crit Care Med. 2017 Jan;45(1):e77-e85</Citation><ArticleIdList><ArticleId IdType="pubmed">27618275</ArticleId></ArticleIdList></Reference><Reference><Citation>Front Microbiol. 2018 Jul 25;9:1612</Citation><ArticleIdList><ArticleId IdType="pubmed">30090091</ArticleId></ArticleIdList></Reference><Reference><Citation>J Immunol. 2009 Apr 1;182(7):4046-55</Citation><ArticleIdList><ArticleId IdType="pubmed">19299702</ArticleId></ArticleIdList></Reference><Reference><Citation>BMC Res Notes. 2014 Apr 12;7:233</Citation><ArticleIdList><ArticleId IdType="pubmed">24725742</ArticleId></ArticleIdList></Reference><Reference><Citation>Mycoses. 2005 May;48(3):151-61</Citation><ArticleIdList><ArticleId IdType="pubmed">15842329</ArticleId></ArticleIdList></Reference><Reference><Citation>FEBS J. 2015 Dec;282(24):4672-8</Citation><ArticleIdList><ArticleId IdType="pubmed">26432171</ArticleId></ArticleIdList></Reference><Reference><Citation>Nat Rev Cancer. 2018 Dec;18(12):744-757</Citation><ArticleIdList><ArticleId IdType="pubmed">30425336</ArticleId></ArticleIdList></Reference><Reference><Citation>Virulence. 2015;6(4):316-26</Citation><ArticleIdList><ArticleId IdType="pubmed">25785541</ArticleId></ArticleIdList></Reference><Reference><Citation>PLoS One. 2014 Jul 16;9(7):e102066</Citation><ArticleIdList><ArticleId IdType="pubmed">25029098</ArticleId></ArticleIdList></Reference><Reference><Citation>Ann Immunol (Paris). 1980 Jan-Feb;131C(1):93-104</Citation><ArticleIdList><ArticleId IdType="pubmed">7396418</ArticleId></ArticleIdList></Reference><Reference><Citation>Nat Rev Immunol. 2012 Apr 20;12(5):325-38</Citation><ArticleIdList><ArticleId IdType="pubmed">22517423</ArticleId></ArticleIdList></Reference><Reference><Citation>Curr Biol. 2003 Aug 5;13(15):1259-68</Citation><ArticleIdList><ArticleId IdType="pubmed">12906785</ArticleId></ArticleIdList></Reference><Reference><Citation>Science. 2016 Jan 1;351(6268):48-52</Citation><ArticleIdList><ArticleId IdType="pubmed">26678875</ArticleId></ArticleIdList></Reference><Reference><Citation>Cell Microbiol. 2019 May;21(5):e12995</Citation><ArticleIdList><ArticleId IdType="pubmed">30577088</ArticleId></ArticleIdList></Reference><Reference><Citation>Cell Host Microbe. 2018 Jan 10;23(1):121-133.e4</Citation><ArticleIdList><ArticleId IdType="pubmed">29290576</ArticleId></ArticleIdList></Reference><Reference><Citation>Nat Rev Immunol. 2013 Oct;13(10):722-37</Citation><ArticleIdList><ArticleId IdType="pubmed">24064518</ArticleId></ArticleIdList></Reference><Reference><Citation>Autophagy. 2016;12(1):1-222</Citation><ArticleIdList><ArticleId IdType="pubmed">26799652</ArticleId></ArticleIdList></Reference><Reference><Citation>Curr Top Dev Biol. 2015;114:67-91</Citation><ArticleIdList><ArticleId IdType="pubmed">26431564</ArticleId></ArticleIdList></Reference><Reference><Citation>J Immunol. 2011 Aug 1;187(3):1106-12</Citation><ArticleIdList><ArticleId IdType="pubmed">21709159</ArticleId></ArticleIdList></Reference><Reference><Citation>J Clin Med Res. 2011 Apr 4;3(2):65-71</Citation><ArticleIdList><ArticleId IdType="pubmed">21811532</ArticleId></ArticleIdList></Reference><Reference><Citation>Nat Immunol. 2011 Apr;12(4):295-303</Citation><ArticleIdList><ArticleId IdType="pubmed">21358638</ArticleId></ArticleIdList></Reference><Reference><Citation>Clin Infect Dis. 2016 Feb 15;62(4):e1-50</Citation><ArticleIdList><ArticleId IdType="pubmed">26679628</ArticleId></ArticleIdList></Reference><Reference><Citation>Mediators Inflamm. 2017;2017:4926205</Citation><ArticleIdList><ArticleId IdType="pubmed">29358849</ArticleId></ArticleIdList></Reference><Reference><Citation>N Engl J Med. 2015 Oct 8;373(15):1445-56</Citation><ArticleIdList><ArticleId IdType="pubmed">26444731</ArticleId></ArticleIdList></Reference><Reference><Citation>Cell. 2014 Mar 27;157(1):65-75</Citation><ArticleIdList><ArticleId IdType="pubmed">24679527</ArticleId></ArticleIdList></Reference><Reference><Citation>Am J Cancer Res. 2012;2(4):397-413</Citation><ArticleIdList><ArticleId IdType="pubmed">22860231</ArticleId></ArticleIdList></Reference><Reference><Citation>Crit Care. 2016 Jan 20;20:15</Citation><ArticleIdList><ArticleId IdType="pubmed">26786705</ArticleId></ArticleIdList></Reference><Reference><Citation>Ann Gastroenterol Surg. 2018 Jul 24;2(5):351-358</Citation><ArticleIdList><ArticleId IdType="pubmed">30238076</ArticleId></ArticleIdList></Reference><Reference><Citation>J Intensive Care Med. 2018 Sep 19;:885066618800690</Citation><ArticleIdList><ArticleId IdType="pubmed">30231674</ArticleId></ArticleIdList></Reference><Reference><Citation>Curr Opin Cell Biol. 2017 Apr;45:72-82</Citation><ArticleIdList><ArticleId IdType="pubmed">28411448</ArticleId></ArticleIdList></Reference><Reference><Citation>Eur J Immunol. 2011 Nov;41(11):3361-70</Citation><ArticleIdList><ArticleId IdType="pubmed">21805467</ArticleId></ArticleIdList></Reference><Reference><Citation>Chin Med J (Engl). 2016 Jul 20;129(14):1704-10</Citation><ArticleIdList><ArticleId IdType="pubmed">27411458</ArticleId></ArticleIdList></Reference><Reference><Citation>Rev Esp Quimioter. 2017 Dec;30(6):397-406</Citation><ArticleIdList><ArticleId IdType="pubmed">29115366</ArticleId></ArticleIdList></Reference><Reference><Citation>Cell Death Differ. 2009 Jul;16(7):966-75</Citation><ArticleIdList><ArticleId IdType="pubmed">19325568</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></pubmed><affiliations><list><country><li>République populaire de Chine</li></country><settlement><li>Pékin</li></settlement></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Wang, Hao" sort="Wang, Hao" uniqKey="Wang H" first="Hao" last="Wang">Hao Wang</name></noRegion><name sortKey="Bai, Guangxu" sort="Bai, Guangxu" uniqKey="Bai G" first="Guangxu" last="Bai">Guangxu Bai</name><name sortKey="Cui, Na" sort="Cui, Na" uniqKey="Cui N" first="Na" last="Cui">Na Cui</name><name sortKey="Cui, Na" sort="Cui, Na" uniqKey="Cui N" first="Na" last="Cui">Na Cui</name><name sortKey="Han, Wen" sort="Han, Wen" uniqKey="Han W" first="Wen" last="Han">Wen Han</name><name sortKey="Long, Yun" sort="Long, Yun" uniqKey="Long Y" first="Yun" last="Long">Yun Long</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Bois/explor/RapamycinFungusV1/Data/Main/Exploration
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000222 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd -nk 000222 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Bois
|area= RapamycinFungusV1
|flux= Main
|étape= Exploration
|type= RBID
|clé= pubmed:31668132
|texte= T-cell-specific mTOR deletion in mice ameliorated CD4+ T-cell survival in lethal sepsis induced by severe invasive candidiasis.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Exploration/RBID.i -Sk "pubmed:31668132" \
| HfdSelect -Kh $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd \
| NlmPubMed2Wicri -a RapamycinFungusV1
| This area was generated with Dilib version V0.6.38. |  |