RapamycinFungusV1, Main, Exploration, bibRecord, 000666

Active mTORC2 Signaling in Naive T Cells Suppresses Bone Marrow Homing by Inhibiting CXCR4 Expression.

Identifieur interne : 000666 ( Main/Exploration ); précédent : 000665; suivant : 000667

Active mTORC2 Signaling in Naive T Cells Suppresses Bone Marrow Homing by Inhibiting CXCR4 Expression.

Auteurs : Omotooke A. Arojo [États-Unis] ; Xinxing Ouyang [États-Unis] ; Dou Liu [États-Unis, République populaire de Chine] ; Ting Meng [États-Unis] ; Susan M. Kaech [États-Unis] ; Joao P. Pereira [États-Unis] ; Bing Su [États-Unis, République populaire de Chine]

Source :

Journal of immunology (Baltimore, Md. : 1950) [ 1550-6606 ] ; 2018.

RBID : pubmed:29934471

Descripteurs français

English descriptors

KwdEn :
- Animals (MeSH), Bone Marrow (immunology), Bone Marrow (metabolism), Carrier Proteins (metabolism), Chemokine CXCL12 (metabolism), Forkhead Box Protein O1 (metabolism), Homeostasis (immunology), Mechanistic Target of Rapamycin Complex 2 (metabolism), Mice (MeSH), Mice, Inbred C57BL (MeSH), Receptors, CXCR4 (metabolism), Signal Transduction (immunology), T-Lymphocytes (immunology), T-Lymphocytes (metabolism).
MESH :
- chemical , metabolism : Carrier Proteins, Chemokine CXCL12, Forkhead Box Protein O1, Mechanistic Target of Rapamycin Complex 2, Receptors, CXCR4.
- immunology : Bone Marrow, Homeostasis, Signal Transduction, T-Lymphocytes.
- metabolism : Bone Marrow, T-Lymphocytes.
- Animals, Mice, Mice, Inbred C57BL.

Abstract

Recirculation of naive T cells between secondary lymphoid organs to receive survival cues and scan for signs of infection or other pathologic conditions is important for immune homeostasis and effective immune responses. Although the mechanisms that specifically guide the entry of naive T cells into secondary lymphoid organs are well studied, the mechanisms that keep them from fluxing into inappropriate or undesirable compartments, such as healthy tissues or bone marrow, are less well understood. In this study, we report an unexpected finding that under steady state, bone marrow homing of naive T cells is actively suppressed by mTORC2 signaling. We found that in mice, T cell-specific deletion of an essential mTORC2 component Sin1 results in increased accumulation of naive T cells in the bone marrow. Mechanistically, we show that loss of mTORC2 signaling in naive T cells results in enhanced FOXO1 activity, which leads to increased CXCR4 expression and chemotactic response to CXCL12, a key chemokine that promotes bone marrow homing and retention of T cells. Together, the results of our study reveal a novel role of mTORC2 in T cell homeostasis via active suppression of naive T cell bone marrow homing by the mTORC2-FOXO1-CXCR4 axis.

DOI: 10.4049/jimmunol.1800529
PubMed: 29934471

Affiliations:

Links toward previous steps (curation, corpus...)

to stream Main, to step Corpus: 000519
to stream Main, to step Curation: 000519

Le document en format XML

<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Active mTORC2 Signaling in Naive T Cells Suppresses Bone Marrow Homing by Inhibiting CXCR4 Expression.</title>
<author><name sortKey="Arojo, Omotooke A" sort="Arojo, Omotooke A" uniqKey="Arojo O" first="Omotooke A" last="Arojo">Omotooke A. Arojo</name>
<affiliation wicri:level="2"><nlm:affiliation>Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06519.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Connecticut</region>
</placeName>
<wicri:cityArea>Department of Immunobiology, Yale University School of Medicine, New Haven</wicri:cityArea>
</affiliation>
</author>
<author><name sortKey="Ouyang, Xinxing" sort="Ouyang, Xinxing" uniqKey="Ouyang X" first="Xinxing" last="Ouyang">Xinxing Ouyang</name>
<affiliation wicri:level="2"><nlm:affiliation>Vascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, CT 06519; and.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Connecticut</region>
</placeName>
<wicri:cityArea>Vascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven</wicri:cityArea>
</affiliation>
</author>
<author><name sortKey="Liu, Dou" sort="Liu, Dou" uniqKey="Liu D" first="Dou" last="Liu">Dou Liu</name>
<affiliation wicri:level="2"><nlm:affiliation>Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06519.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Connecticut</region>
</placeName>
<wicri:cityArea>Department of Immunobiology, Yale University School of Medicine, New Haven</wicri:cityArea>
</affiliation>
<affiliation wicri:level="1"><nlm:affiliation>Department of Microbiology and Immunology, Shanghai Institute of Immunology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Microbiology and Immunology, Shanghai Institute of Immunology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025</wicri:regionArea>
<wicri:noRegion>Shanghai 200025</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Meng, Ting" sort="Meng, Ting" uniqKey="Meng T" first="Ting" last="Meng">Ting Meng</name>
<affiliation wicri:level="2"><nlm:affiliation>Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06519.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Connecticut</region>
</placeName>
<wicri:cityArea>Department of Immunobiology, Yale University School of Medicine, New Haven</wicri:cityArea>
</affiliation>
</author>
<author><name sortKey="Kaech, Susan M" sort="Kaech, Susan M" uniqKey="Kaech S" first="Susan M" last="Kaech">Susan M. Kaech</name>
<affiliation wicri:level="2"><nlm:affiliation>Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06519.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Connecticut</region>
</placeName>
<wicri:cityArea>Department of Immunobiology, Yale University School of Medicine, New Haven</wicri:cityArea>
</affiliation>
</author>
<author><name sortKey="Pereira, Joao P" sort="Pereira, Joao P" uniqKey="Pereira J" first="Joao P" last="Pereira">Joao P. Pereira</name>
<affiliation wicri:level="2"><nlm:affiliation>Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06519.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Connecticut</region>
</placeName>
<wicri:cityArea>Department of Immunobiology, Yale University School of Medicine, New Haven</wicri:cityArea>
</affiliation>
</author>
<author><name sortKey="Su, Bing" sort="Su, Bing" uniqKey="Su B" first="Bing" last="Su">Bing Su</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06519; bing.su@yale.edu.</nlm:affiliation>
<country wicri:rule="url">États-Unis</country>
<wicri:regionArea>Department of Immunobiology, Yale University School of Medicine, New Haven</wicri:regionArea>
<wicri:noRegion>New Haven</wicri:noRegion>
</affiliation>
<affiliation wicri:level="2"><nlm:affiliation>Vascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, CT 06519; and.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Connecticut</region>
</placeName>
<wicri:cityArea>Vascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven</wicri:cityArea>
</affiliation>
<affiliation wicri:level="1"><nlm:affiliation>Department of Microbiology and Immunology, Shanghai Institute of Immunology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Microbiology and Immunology, Shanghai Institute of Immunology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025</wicri:regionArea>
<wicri:noRegion>Shanghai 200025</wicri:noRegion>
</affiliation>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">PubMed</idno>
<date when="2018">2018</date>
<idno type="RBID">pubmed:29934471</idno>
<idno type="pmid">29934471</idno>
<idno type="doi">10.4049/jimmunol.1800529</idno>
<idno type="wicri:Area/Main/Corpus">000519</idno>
<idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000519</idno>
<idno type="wicri:Area/Main/Curation">000519</idno>
<idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Curation">000519</idno>
<idno type="wicri:Area/Main/Exploration">000519</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title xml:lang="en">Active mTORC2 Signaling in Naive T Cells Suppresses Bone Marrow Homing by Inhibiting CXCR4 Expression.</title>
<author><name sortKey="Arojo, Omotooke A" sort="Arojo, Omotooke A" uniqKey="Arojo O" first="Omotooke A" last="Arojo">Omotooke A. Arojo</name>
<affiliation wicri:level="2"><nlm:affiliation>Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06519.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Connecticut</region>
</placeName>
<wicri:cityArea>Department of Immunobiology, Yale University School of Medicine, New Haven</wicri:cityArea>
</affiliation>
</author>
<author><name sortKey="Ouyang, Xinxing" sort="Ouyang, Xinxing" uniqKey="Ouyang X" first="Xinxing" last="Ouyang">Xinxing Ouyang</name>
<affiliation wicri:level="2"><nlm:affiliation>Vascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, CT 06519; and.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Connecticut</region>
</placeName>
<wicri:cityArea>Vascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven</wicri:cityArea>
</affiliation>
</author>
<author><name sortKey="Liu, Dou" sort="Liu, Dou" uniqKey="Liu D" first="Dou" last="Liu">Dou Liu</name>
<affiliation wicri:level="2"><nlm:affiliation>Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06519.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Connecticut</region>
</placeName>
<wicri:cityArea>Department of Immunobiology, Yale University School of Medicine, New Haven</wicri:cityArea>
</affiliation>
<affiliation wicri:level="1"><nlm:affiliation>Department of Microbiology and Immunology, Shanghai Institute of Immunology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Microbiology and Immunology, Shanghai Institute of Immunology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025</wicri:regionArea>
<wicri:noRegion>Shanghai 200025</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Meng, Ting" sort="Meng, Ting" uniqKey="Meng T" first="Ting" last="Meng">Ting Meng</name>
<affiliation wicri:level="2"><nlm:affiliation>Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06519.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Connecticut</region>
</placeName>
<wicri:cityArea>Department of Immunobiology, Yale University School of Medicine, New Haven</wicri:cityArea>
</affiliation>
</author>
<author><name sortKey="Kaech, Susan M" sort="Kaech, Susan M" uniqKey="Kaech S" first="Susan M" last="Kaech">Susan M. Kaech</name>
<affiliation wicri:level="2"><nlm:affiliation>Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06519.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Connecticut</region>
</placeName>
<wicri:cityArea>Department of Immunobiology, Yale University School of Medicine, New Haven</wicri:cityArea>
</affiliation>
</author>
<author><name sortKey="Pereira, Joao P" sort="Pereira, Joao P" uniqKey="Pereira J" first="Joao P" last="Pereira">Joao P. Pereira</name>
<affiliation wicri:level="2"><nlm:affiliation>Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06519.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Connecticut</region>
</placeName>
<wicri:cityArea>Department of Immunobiology, Yale University School of Medicine, New Haven</wicri:cityArea>
</affiliation>
</author>
<author><name sortKey="Su, Bing" sort="Su, Bing" uniqKey="Su B" first="Bing" last="Su">Bing Su</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06519; bing.su@yale.edu.</nlm:affiliation>
<country wicri:rule="url">États-Unis</country>
<wicri:regionArea>Department of Immunobiology, Yale University School of Medicine, New Haven</wicri:regionArea>
<wicri:noRegion>New Haven</wicri:noRegion>
</affiliation>
<affiliation wicri:level="2"><nlm:affiliation>Vascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, CT 06519; and.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Connecticut</region>
</placeName>
<wicri:cityArea>Vascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven</wicri:cityArea>
</affiliation>
<affiliation wicri:level="1"><nlm:affiliation>Department of Microbiology and Immunology, Shanghai Institute of Immunology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Microbiology and Immunology, Shanghai Institute of Immunology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025</wicri:regionArea>
<wicri:noRegion>Shanghai 200025</wicri:noRegion>
</affiliation>
</author>
</analytic>
<series><title level="j">Journal of immunology (Baltimore, Md. : 1950)</title>
<idno type="eISSN">1550-6606</idno>
<imprint><date when="2018" type="published">2018</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term>
<term>Bone Marrow (immunology)</term>
<term>Bone Marrow (metabolism)</term>
<term>Carrier Proteins (metabolism)</term>
<term>Chemokine CXCL12 (metabolism)</term>
<term>Forkhead Box Protein O1 (metabolism)</term>
<term>Homeostasis (immunology)</term>
<term>Mechanistic Target of Rapamycin Complex 2 (metabolism)</term>
<term>Mice (MeSH)</term>
<term>Mice, Inbred C57BL (MeSH)</term>
<term>Receptors, CXCR4 (metabolism)</term>
<term>Signal Transduction (immunology)</term>
<term>T-Lymphocytes (immunology)</term>
<term>T-Lymphocytes (metabolism)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term>
<term>Chimiokine CXCL12 (métabolisme)</term>
<term>Complexe-2 cible mécanistique de la rapamycine (métabolisme)</term>
<term>Homéostasie (immunologie)</term>
<term>Lymphocytes T (immunologie)</term>
<term>Lymphocytes T (métabolisme)</term>
<term>Moelle osseuse (immunologie)</term>
<term>Moelle osseuse (métabolisme)</term>
<term>Protéine O1 à motif en tête de fourche (métabolisme)</term>
<term>Protéines de transport (métabolisme)</term>
<term>Récepteurs CXCR4 (métabolisme)</term>
<term>Souris (MeSH)</term>
<term>Souris de lignée C57BL (MeSH)</term>
<term>Transduction du signal (immunologie)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Carrier Proteins</term>
<term>Chemokine CXCL12</term>
<term>Forkhead Box Protein O1</term>
<term>Mechanistic Target of Rapamycin Complex 2</term>
<term>Receptors, CXCR4</term>
</keywords>
<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Homéostasie</term>
<term>Lymphocytes T</term>
<term>Moelle osseuse</term>
<term>Transduction du signal</term>
</keywords>
<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Bone Marrow</term>
<term>Homeostasis</term>
<term>Signal Transduction</term>
<term>T-Lymphocytes</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Bone Marrow</term>
<term>T-Lymphocytes</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Chimiokine CXCL12</term>
<term>Complexe-2 cible mécanistique de la rapamycine</term>
<term>Lymphocytes T</term>
<term>Moelle osseuse</term>
<term>Protéine O1 à motif en tête de fourche</term>
<term>Protéines de transport</term>
<term>Récepteurs CXCR4</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Souris</term>
<term>Souris de lignée C57BL</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">Recirculation of naive T cells between secondary lymphoid organs to receive survival cues and scan for signs of infection or other pathologic conditions is important for immune homeostasis and effective immune responses. Although the mechanisms that specifically guide the entry of naive T cells into secondary lymphoid organs are well studied, the mechanisms that keep them from fluxing into inappropriate or undesirable compartments, such as healthy tissues or bone marrow, are less well understood. In this study, we report an unexpected finding that under steady state, bone marrow homing of naive T cells is actively suppressed by mTORC2 signaling. We found that in mice, T cell-specific deletion of an essential mTORC2 component Sin1 results in increased accumulation of naive T cells in the bone marrow. Mechanistically, we show that loss of mTORC2 signaling in naive T cells results in enhanced FOXO1 activity, which leads to increased CXCR4 expression and chemotactic response to CXCL12, a key chemokine that promotes bone marrow homing and retention of T cells. Together, the results of our study reveal a novel role of mTORC2 in T cell homeostasis via active suppression of naive T cell bone marrow homing by the mTORC2-FOXO1-CXCR4 axis.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">29934471</PMID>
<DateCompleted><Year>2019</Year>
<Month>06</Month>
<Day>21</Day>
</DateCompleted>
<DateRevised><Year>2019</Year>
<Month>06</Month>
<Day>21</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1550-6606</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>201</Volume>
<Issue>3</Issue>
<PubDate><Year>2018</Year>
<Month>08</Month>
<Day>01</Day>
</PubDate>
</JournalIssue>
<Title>Journal of immunology (Baltimore, Md. : 1950)</Title>
<ISOAbbreviation>J Immunol</ISOAbbreviation>
</Journal>
<ArticleTitle>Active mTORC2 Signaling in Naive T Cells Suppresses Bone Marrow Homing by Inhibiting CXCR4 Expression.</ArticleTitle>
<Pagination><MedlinePgn>908-915</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.4049/jimmunol.1800529</ELocationID>
<Abstract><AbstractText>Recirculation of naive T cells between secondary lymphoid organs to receive survival cues and scan for signs of infection or other pathologic conditions is important for immune homeostasis and effective immune responses. Although the mechanisms that specifically guide the entry of naive T cells into secondary lymphoid organs are well studied, the mechanisms that keep them from fluxing into inappropriate or undesirable compartments, such as healthy tissues or bone marrow, are less well understood. In this study, we report an unexpected finding that under steady state, bone marrow homing of naive T cells is actively suppressed by mTORC2 signaling. We found that in mice, T cell-specific deletion of an essential mTORC2 component Sin1 results in increased accumulation of naive T cells in the bone marrow. Mechanistically, we show that loss of mTORC2 signaling in naive T cells results in enhanced FOXO1 activity, which leads to increased CXCR4 expression and chemotactic response to CXCL12, a key chemokine that promotes bone marrow homing and retention of T cells. Together, the results of our study reveal a novel role of mTORC2 in T cell homeostasis via active suppression of naive T cell bone marrow homing by the mTORC2-FOXO1-CXCR4 axis.</AbstractText>
<CopyrightInformation>Copyright © 2018 by The American Association of Immunologists, Inc.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Arojo</LastName>
<ForeName>Omotooke A</ForeName>
<Initials>OA</Initials>
<AffiliationInfo><Affiliation>Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06519.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Ouyang</LastName>
<ForeName>Xinxing</ForeName>
<Initials>X</Initials>
<AffiliationInfo><Affiliation>Vascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, CT 06519; and.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Liu</LastName>
<ForeName>Dou</ForeName>
<Initials>D</Initials>
<AffiliationInfo><Affiliation>Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06519.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Microbiology and Immunology, Shanghai Institute of Immunology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Meng</LastName>
<ForeName>Ting</ForeName>
<Initials>T</Initials>
<AffiliationInfo><Affiliation>Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06519.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Kaech</LastName>
<ForeName>Susan M</ForeName>
<Initials>SM</Initials>
<AffiliationInfo><Affiliation>Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06519.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Pereira</LastName>
<ForeName>Joao P</ForeName>
<Initials>JP</Initials>
<Identifier Source="ORCID">0000-0002-5694-4938</Identifier>
<AffiliationInfo><Affiliation>Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06519.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Su</LastName>
<ForeName>Bing</ForeName>
<Initials>B</Initials>
<AffiliationInfo><Affiliation>Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06519; bing.su@yale.edu.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Vascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, CT 06519; and.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Microbiology and Immunology, Shanghai Institute of Immunology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><GrantID>R01 GM114621</GrantID>
<Acronym>GM</Acronym>
<Agency>NIGMS NIH HHS</Agency>
<Country>United States</Country>
</Grant>
</GrantList>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
<PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType>
<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2018</Year>
<Month>06</Month>
<Day>22</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>United States</Country>
<MedlineTA>J Immunol</MedlineTA>
<NlmUniqueID>2985117R</NlmUniqueID>
<ISSNLinking>0022-1767</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C514936">CXCR4 protein, mouse</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D002352">Carrier Proteins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D054377">Chemokine CXCL12</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000071161">Forkhead Box Protein O1</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D019718">Receptors, CXCR4</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber>
<NameOfSubstance UI="D000076225">Mechanistic Target of Rapamycin Complex 2</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>AIM</CitationSubset>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D001853" MajorTopicYN="N">Bone Marrow</DescriptorName>
<QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002352" MajorTopicYN="N">Carrier Proteins</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D054377" MajorTopicYN="N">Chemokine CXCL12</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000071161" MajorTopicYN="N">Forkhead Box Protein O1</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006706" MajorTopicYN="N">Homeostasis</DescriptorName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000076225" MajorTopicYN="N">Mechanistic Target of Rapamycin Complex 2</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D019718" MajorTopicYN="N">Receptors, CXCR4</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName>
<QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D013601" MajorTopicYN="N">T-Lymphocytes</DescriptorName>
<QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
</MeshHeadingList>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2018</Year>
<Month>04</Month>
<Day>12</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted"><Year>2018</Year>
<Month>05</Month>
<Day>25</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="pubmed"><Year>2018</Year>
<Month>6</Month>
<Day>24</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="medline"><Year>2019</Year>
<Month>6</Month>
<Day>22</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="entrez"><Year>2018</Year>
<Month>6</Month>
<Day>24</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
</History>
<PublicationStatus>ppublish</PublicationStatus>
<ArticleIdList><ArticleId IdType="pubmed">29934471</ArticleId>
<ArticleId IdType="pii">jimmunol.1800529</ArticleId>
<ArticleId IdType="doi">10.4049/jimmunol.1800529</ArticleId>
</ArticleIdList>
</PubmedData>
</pubmed>
<affiliations><list><country><li>République populaire de Chine</li>
<li>États-Unis</li>
</country>
<region><li>Connecticut</li>
</region>
</list>
<tree><country name="États-Unis"><region name="Connecticut"><name sortKey="Arojo, Omotooke A" sort="Arojo, Omotooke A" uniqKey="Arojo O" first="Omotooke A" last="Arojo">Omotooke A. Arojo</name>
</region>
<name sortKey="Kaech, Susan M" sort="Kaech, Susan M" uniqKey="Kaech S" first="Susan M" last="Kaech">Susan M. Kaech</name>
<name sortKey="Liu, Dou" sort="Liu, Dou" uniqKey="Liu D" first="Dou" last="Liu">Dou Liu</name>
<name sortKey="Meng, Ting" sort="Meng, Ting" uniqKey="Meng T" first="Ting" last="Meng">Ting Meng</name>
<name sortKey="Ouyang, Xinxing" sort="Ouyang, Xinxing" uniqKey="Ouyang X" first="Xinxing" last="Ouyang">Xinxing Ouyang</name>
<name sortKey="Pereira, Joao P" sort="Pereira, Joao P" uniqKey="Pereira J" first="Joao P" last="Pereira">Joao P. Pereira</name>
<name sortKey="Su, Bing" sort="Su, Bing" uniqKey="Su B" first="Bing" last="Su">Bing Su</name>
<name sortKey="Su, Bing" sort="Su, Bing" uniqKey="Su B" first="Bing" last="Su">Bing Su</name>
</country>
<country name="République populaire de Chine"><noRegion><name sortKey="Liu, Dou" sort="Liu, Dou" uniqKey="Liu D" first="Dou" last="Liu">Dou Liu</name>
</noRegion>
<name sortKey="Su, Bing" sort="Su, Bing" uniqKey="Su B" first="Bing" last="Su">Bing Su</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 000666 | SxmlIndent | more

HfdSelect -h $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd -nk 000666 | 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:29934471
   |texte=   Active mTORC2 Signaling in Naive T Cells Suppresses Bone Marrow Homing by Inhibiting CXCR4 Expression.
}}

Pour générer des pages wiki

HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Exploration/RBID.i   -Sk "pubmed:29934471" \
       | HfdSelect -Kh $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd   \
       | NlmPubMed2Wicri -a RapamycinFungusV1

This area was generated with Dilib version V0.6.38.
Data generation: Thu Nov 19 21:55:41 2020. Site generation: Thu Nov 19 22:00:39 2020

	Serveur d'exploration sur la rapamycine et les champignons
	Attention, ce site est en cours de développement ! Attention, site généré par des moyens informatiques à partir de corpus bruts. Les informations ne sont donc pas validées.

Serveur d'exploration sur la rapamycine et les champignons

Active mTORC2 Signaling in Naive T Cells Suppresses Bone Marrow Homing by Inhibiting CXCR4 Expression.

Active mTORC2 Signaling in Naive T Cells Suppresses Bone Marrow Homing by Inhibiting CXCR4 Expression.

Source :

Descripteurs français

English descriptors

Abstract

Links toward previous steps (curation, corpus...)

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri

Pour générer des pages wiki