Control of peripheral tolerance by regulatory T cell-intrinsic Notch signaling.
Identifieur interne : 000D24 ( Main/Exploration ); précédent : 000D23; suivant : 000D25Control of peripheral tolerance by regulatory T cell-intrinsic Notch signaling.
Auteurs : Louis-Marie Charbonnier [États-Unis] ; Sen Wang [États-Unis] ; Peter Georgiev [États-Unis] ; Esen Sefik [États-Unis] ; Talal A. Chatila [États-Unis]Source :
- Nature immunology [ 1529-2916 ] ; 2015.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Compagnon de mTOR insensible à la rapamycine (MeSH), Facteurs de transcription Forkhead (génétique), Facteurs de transcription Forkhead (immunologie), Femelle (MeSH), Lymphocytes T régulateurs (immunologie), Lymphocytes auxiliaires Th1 (immunologie), Maladie du greffon contre l'hôte (immunologie), Maladie du greffon contre l'hôte (prévention et contrôle), Mutation (MeSH), Mâle (MeSH), Protéines de fusion recombinantes (génétique), Protéines de fusion recombinantes (immunologie), Protéines de transport (génétique), Protéines de transport (immunologie), Récepteur Notch1 (déficit), Récepteur Notch1 (génétique), Récepteur Notch1 (immunologie), Souris (MeSH), Souris de lignée BALB C (MeSH), Souris de lignée C57BL (MeSH), Souris knockout (MeSH), Souris transgéniques (MeSH), Tolérance périphérique (MeSH), Transcriptome (MeSH), Transduction du signal (immunologie), Épigenèse génétique (MeSH).
- MESH :
- déficit : Récepteur Notch1.
- génétique : Facteurs de transcription Forkhead, Protéines de fusion recombinantes, Protéines de transport, Récepteur Notch1.
- immunologie : Facteurs de transcription Forkhead, Lymphocytes T régulateurs, Lymphocytes auxiliaires Th1, Maladie du greffon contre l'hôte, Protéines de fusion recombinantes, Protéines de transport, Récepteur Notch1, Transduction du signal.
- prévention et contrôle : Maladie du greffon contre l'hôte.
- Animaux, Compagnon de mTOR insensible à la rapamycine, Femelle, Mutation, Mâle, Souris, Souris de lignée BALB C, Souris de lignée C57BL, Souris knockout, Souris transgéniques, Tolérance périphérique, Transcriptome, Épigenèse génétique.
English descriptors
- KwdEn :
- Animals (MeSH), Carrier Proteins (genetics), Carrier Proteins (immunology), Epigenesis, Genetic (MeSH), Female (MeSH), Forkhead Transcription Factors (genetics), Forkhead Transcription Factors (immunology), Graft vs Host Disease (immunology), Graft vs Host Disease (prevention & control), Male (MeSH), Mice (MeSH), Mice, Inbred BALB C (MeSH), Mice, Inbred C57BL (MeSH), Mice, Knockout (MeSH), Mice, Transgenic (MeSH), Mutation (MeSH), Peripheral Tolerance (MeSH), Rapamycin-Insensitive Companion of mTOR Protein (MeSH), Receptor, Notch1 (deficiency), Receptor, Notch1 (genetics), Receptor, Notch1 (immunology), Recombinant Fusion Proteins (genetics), Recombinant Fusion Proteins (immunology), Signal Transduction (immunology), T-Lymphocytes, Regulatory (immunology), Th1 Cells (immunology), Transcriptome (MeSH).
- MESH :
- chemical , deficiency : Receptor, Notch1.
- chemical , genetics : Carrier Proteins, Forkhead Transcription Factors, Receptor, Notch1, Recombinant Fusion Proteins.
- chemical , immunology : Carrier Proteins, Forkhead Transcription Factors, Receptor, Notch1, Recombinant Fusion Proteins.
- immunology : Graft vs Host Disease, Signal Transduction, T-Lymphocytes, Regulatory, Th1 Cells.
- prevention & control : Graft vs Host Disease.
- Animals, Epigenesis, Genetic, Female, Male, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Mice, Knockout, Mice, Transgenic, Mutation, Peripheral Tolerance, Rapamycin-Insensitive Companion of mTOR Protein, Transcriptome.
Abstract
Receptors of the Notch family direct the differentiation of helper T cell subsets, but their influence on regulatory T cell (T(reg) cell) responses is obscure. We found here that lineage-specific deletion of components of the Notch pathway enhanced T(reg) cell-mediated suppression of type 1 helper T cell (T(H)1 cell) responses and protected against their T(H)1 skewing and apoptosis. In contrast, expression in T(reg) cells of a gain-of-function transgene encoding the Notch1 intracellular domain resulted in lymphoproliferation, exacerbated T(H)1 responses and autoimmunity. Cell-intrinsic canonical Notch signaling impaired T(reg) cell fitness and promoted the acquisition by T(reg) cells of a T(H)1 cell-like phenotype, whereas non-canonical Notch signaling dependent on the adaptor Rictor activated the kinase AKT-transcription factor Foxo1 axis and impaired the epigenetic stability of Foxp3. Our findings establish a critical role for Notch signaling in controlling peripheral T(reg) cell function.
DOI: 10.1038/ni.3288
PubMed: 26437242
PubMed Central: PMC4618075
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Control of peripheral tolerance by regulatory T cell-intrinsic Notch signaling.</title>
<author><name sortKey="Charbonnier, Louis Marie" sort="Charbonnier, Louis Marie" uniqKey="Charbonnier L" first="Louis-Marie" last="Charbonnier">Louis-Marie Charbonnier</name>
<affiliation wicri:level="2"><nlm:affiliation>Division of Immunology, Boston Children's Hospital, Department of Pediatrics, Harvard Medical School, Boston, Massachusetts, USA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Division of Immunology, Boston Children's Hospital, Department of Pediatrics, Harvard Medical School, Boston, Massachusetts</wicri:regionArea>
<placeName><region type="state">Massachusetts</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Wang, Sen" sort="Wang, Sen" uniqKey="Wang S" first="Sen" last="Wang">Sen Wang</name>
<affiliation wicri:level="2"><nlm:affiliation>Division of Immunology, Boston Children's Hospital, Department of Pediatrics, Harvard Medical School, Boston, Massachusetts, USA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Division of Immunology, Boston Children's Hospital, Department of Pediatrics, Harvard Medical School, Boston, Massachusetts</wicri:regionArea>
<placeName><region type="state">Massachusetts</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Georgiev, Peter" sort="Georgiev, Peter" uniqKey="Georgiev P" first="Peter" last="Georgiev">Peter Georgiev</name>
<affiliation wicri:level="2"><nlm:affiliation>Division of Immunology, Boston Children's Hospital, Department of Pediatrics, Harvard Medical School, Boston, Massachusetts, USA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Division of Immunology, Boston Children's Hospital, Department of Pediatrics, Harvard Medical School, Boston, Massachusetts</wicri:regionArea>
<placeName><region type="state">Massachusetts</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Sefik, Esen" sort="Sefik, Esen" uniqKey="Sefik E" first="Esen" last="Sefik">Esen Sefik</name>
<affiliation wicri:level="2"><nlm:affiliation>Division of Immunology, Department of Microbiology and Immunobiology, Harvard Medical School, Boston, Massachusetts, USA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Division of Immunology, Department of Microbiology and Immunobiology, Harvard Medical School, Boston, Massachusetts</wicri:regionArea>
<placeName><region type="state">Massachusetts</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Chatila, Talal A" sort="Chatila, Talal A" uniqKey="Chatila T" first="Talal A" last="Chatila">Talal A. Chatila</name>
<affiliation wicri:level="2"><nlm:affiliation>Division of Immunology, Boston Children's Hospital, Department of Pediatrics, Harvard Medical School, Boston, Massachusetts, USA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Division of Immunology, Boston Children's Hospital, Department of Pediatrics, Harvard Medical School, Boston, Massachusetts</wicri:regionArea>
<placeName><region type="state">Massachusetts</region>
</placeName>
</affiliation>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">PubMed</idno>
<date when="2015">2015</date>
<idno type="RBID">pubmed:26437242</idno>
<idno type="pmid">26437242</idno>
<idno type="doi">10.1038/ni.3288</idno>
<idno type="pmc">PMC4618075</idno>
<idno type="wicri:Area/Main/Corpus">000B72</idno>
<idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000B72</idno>
<idno type="wicri:Area/Main/Curation">000B72</idno>
<idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Curation">000B72</idno>
<idno type="wicri:Area/Main/Exploration">000B72</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title xml:lang="en">Control of peripheral tolerance by regulatory T cell-intrinsic Notch signaling.</title>
<author><name sortKey="Charbonnier, Louis Marie" sort="Charbonnier, Louis Marie" uniqKey="Charbonnier L" first="Louis-Marie" last="Charbonnier">Louis-Marie Charbonnier</name>
<affiliation wicri:level="2"><nlm:affiliation>Division of Immunology, Boston Children's Hospital, Department of Pediatrics, Harvard Medical School, Boston, Massachusetts, USA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Division of Immunology, Boston Children's Hospital, Department of Pediatrics, Harvard Medical School, Boston, Massachusetts</wicri:regionArea>
<placeName><region type="state">Massachusetts</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Wang, Sen" sort="Wang, Sen" uniqKey="Wang S" first="Sen" last="Wang">Sen Wang</name>
<affiliation wicri:level="2"><nlm:affiliation>Division of Immunology, Boston Children's Hospital, Department of Pediatrics, Harvard Medical School, Boston, Massachusetts, USA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Division of Immunology, Boston Children's Hospital, Department of Pediatrics, Harvard Medical School, Boston, Massachusetts</wicri:regionArea>
<placeName><region type="state">Massachusetts</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Georgiev, Peter" sort="Georgiev, Peter" uniqKey="Georgiev P" first="Peter" last="Georgiev">Peter Georgiev</name>
<affiliation wicri:level="2"><nlm:affiliation>Division of Immunology, Boston Children's Hospital, Department of Pediatrics, Harvard Medical School, Boston, Massachusetts, USA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Division of Immunology, Boston Children's Hospital, Department of Pediatrics, Harvard Medical School, Boston, Massachusetts</wicri:regionArea>
<placeName><region type="state">Massachusetts</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Sefik, Esen" sort="Sefik, Esen" uniqKey="Sefik E" first="Esen" last="Sefik">Esen Sefik</name>
<affiliation wicri:level="2"><nlm:affiliation>Division of Immunology, Department of Microbiology and Immunobiology, Harvard Medical School, Boston, Massachusetts, USA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Division of Immunology, Department of Microbiology and Immunobiology, Harvard Medical School, Boston, Massachusetts</wicri:regionArea>
<placeName><region type="state">Massachusetts</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Chatila, Talal A" sort="Chatila, Talal A" uniqKey="Chatila T" first="Talal A" last="Chatila">Talal A. Chatila</name>
<affiliation wicri:level="2"><nlm:affiliation>Division of Immunology, Boston Children's Hospital, Department of Pediatrics, Harvard Medical School, Boston, Massachusetts, USA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Division of Immunology, Boston Children's Hospital, Department of Pediatrics, Harvard Medical School, Boston, Massachusetts</wicri:regionArea>
<placeName><region type="state">Massachusetts</region>
</placeName>
</affiliation>
</author>
</analytic>
<series><title level="j">Nature immunology</title>
<idno type="eISSN">1529-2916</idno>
<imprint><date when="2015" type="published">2015</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term>
<term>Carrier Proteins (genetics)</term>
<term>Carrier Proteins (immunology)</term>
<term>Epigenesis, Genetic (MeSH)</term>
<term>Female (MeSH)</term>
<term>Forkhead Transcription Factors (genetics)</term>
<term>Forkhead Transcription Factors (immunology)</term>
<term>Graft vs Host Disease (immunology)</term>
<term>Graft vs Host Disease (prevention & control)</term>
<term>Male (MeSH)</term>
<term>Mice (MeSH)</term>
<term>Mice, Inbred BALB C (MeSH)</term>
<term>Mice, Inbred C57BL (MeSH)</term>
<term>Mice, Knockout (MeSH)</term>
<term>Mice, Transgenic (MeSH)</term>
<term>Mutation (MeSH)</term>
<term>Peripheral Tolerance (MeSH)</term>
<term>Rapamycin-Insensitive Companion of mTOR Protein (MeSH)</term>
<term>Receptor, Notch1 (deficiency)</term>
<term>Receptor, Notch1 (genetics)</term>
<term>Receptor, Notch1 (immunology)</term>
<term>Recombinant Fusion Proteins (genetics)</term>
<term>Recombinant Fusion Proteins (immunology)</term>
<term>Signal Transduction (immunology)</term>
<term>T-Lymphocytes, Regulatory (immunology)</term>
<term>Th1 Cells (immunology)</term>
<term>Transcriptome (MeSH)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term>
<term>Compagnon de mTOR insensible à la rapamycine (MeSH)</term>
<term>Facteurs de transcription Forkhead (génétique)</term>
<term>Facteurs de transcription Forkhead (immunologie)</term>
<term>Femelle (MeSH)</term>
<term>Lymphocytes T régulateurs (immunologie)</term>
<term>Lymphocytes auxiliaires Th1 (immunologie)</term>
<term>Maladie du greffon contre l'hôte (immunologie)</term>
<term>Maladie du greffon contre l'hôte (prévention et contrôle)</term>
<term>Mutation (MeSH)</term>
<term>Mâle (MeSH)</term>
<term>Protéines de fusion recombinantes (génétique)</term>
<term>Protéines de fusion recombinantes (immunologie)</term>
<term>Protéines de transport (génétique)</term>
<term>Protéines de transport (immunologie)</term>
<term>Récepteur Notch1 (déficit)</term>
<term>Récepteur Notch1 (génétique)</term>
<term>Récepteur Notch1 (immunologie)</term>
<term>Souris (MeSH)</term>
<term>Souris de lignée BALB C (MeSH)</term>
<term>Souris de lignée C57BL (MeSH)</term>
<term>Souris knockout (MeSH)</term>
<term>Souris transgéniques (MeSH)</term>
<term>Tolérance périphérique (MeSH)</term>
<term>Transcriptome (MeSH)</term>
<term>Transduction du signal (immunologie)</term>
<term>Épigenèse génétique (MeSH)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="deficiency" xml:lang="en"><term>Receptor, Notch1</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Carrier Proteins</term>
<term>Forkhead Transcription Factors</term>
<term>Receptor, Notch1</term>
<term>Recombinant Fusion Proteins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Carrier Proteins</term>
<term>Forkhead Transcription Factors</term>
<term>Receptor, Notch1</term>
<term>Recombinant Fusion Proteins</term>
</keywords>
<keywords scheme="MESH" qualifier="déficit" xml:lang="fr"><term>Récepteur Notch1</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Facteurs de transcription Forkhead</term>
<term>Protéines de fusion recombinantes</term>
<term>Protéines de transport</term>
<term>Récepteur Notch1</term>
</keywords>
<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Facteurs de transcription Forkhead</term>
<term>Lymphocytes T régulateurs</term>
<term>Lymphocytes auxiliaires Th1</term>
<term>Maladie du greffon contre l'hôte</term>
<term>Protéines de fusion recombinantes</term>
<term>Protéines de transport</term>
<term>Récepteur Notch1</term>
<term>Transduction du signal</term>
</keywords>
<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Graft vs Host Disease</term>
<term>Signal Transduction</term>
<term>T-Lymphocytes, Regulatory</term>
<term>Th1 Cells</term>
</keywords>
<keywords scheme="MESH" qualifier="prevention & control" xml:lang="en"><term>Graft vs Host Disease</term>
</keywords>
<keywords scheme="MESH" qualifier="prévention et contrôle" xml:lang="fr"><term>Maladie du greffon contre l'hôte</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Epigenesis, Genetic</term>
<term>Female</term>
<term>Male</term>
<term>Mice</term>
<term>Mice, Inbred BALB C</term>
<term>Mice, Inbred C57BL</term>
<term>Mice, Knockout</term>
<term>Mice, Transgenic</term>
<term>Mutation</term>
<term>Peripheral Tolerance</term>
<term>Rapamycin-Insensitive Companion of mTOR Protein</term>
<term>Transcriptome</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Compagnon de mTOR insensible à la rapamycine</term>
<term>Femelle</term>
<term>Mutation</term>
<term>Mâle</term>
<term>Souris</term>
<term>Souris de lignée BALB C</term>
<term>Souris de lignée C57BL</term>
<term>Souris knockout</term>
<term>Souris transgéniques</term>
<term>Tolérance périphérique</term>
<term>Transcriptome</term>
<term>Épigenèse génétique</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">Receptors of the Notch family direct the differentiation of helper T cell subsets, but their influence on regulatory T cell (T(reg) cell) responses is obscure. We found here that lineage-specific deletion of components of the Notch pathway enhanced T(reg) cell-mediated suppression of type 1 helper T cell (T(H)1 cell) responses and protected against their T(H)1 skewing and apoptosis. In contrast, expression in T(reg) cells of a gain-of-function transgene encoding the Notch1 intracellular domain resulted in lymphoproliferation, exacerbated T(H)1 responses and autoimmunity. Cell-intrinsic canonical Notch signaling impaired T(reg) cell fitness and promoted the acquisition by T(reg) cells of a T(H)1 cell-like phenotype, whereas non-canonical Notch signaling dependent on the adaptor Rictor activated the kinase AKT-transcription factor Foxo1 axis and impaired the epigenetic stability of Foxp3. Our findings establish a critical role for Notch signaling in controlling peripheral T(reg) cell function.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26437242</PMID>
<DateCompleted><Year>2016</Year>
<Month>04</Month>
<Day>22</Day>
</DateCompleted>
<DateRevised><Year>2018</Year>
<Month>11</Month>
<Day>13</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1529-2916</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>16</Volume>
<Issue>11</Issue>
<PubDate><Year>2015</Year>
<Month>Nov</Month>
</PubDate>
</JournalIssue>
<Title>Nature immunology</Title>
<ISOAbbreviation>Nat Immunol</ISOAbbreviation>
</Journal>
<ArticleTitle>Control of peripheral tolerance by regulatory T cell-intrinsic Notch signaling.</ArticleTitle>
<Pagination><MedlinePgn>1162-73</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1038/ni.3288</ELocationID>
<Abstract><AbstractText>Receptors of the Notch family direct the differentiation of helper T cell subsets, but their influence on regulatory T cell (T(reg) cell) responses is obscure. We found here that lineage-specific deletion of components of the Notch pathway enhanced T(reg) cell-mediated suppression of type 1 helper T cell (T(H)1 cell) responses and protected against their T(H)1 skewing and apoptosis. In contrast, expression in T(reg) cells of a gain-of-function transgene encoding the Notch1 intracellular domain resulted in lymphoproliferation, exacerbated T(H)1 responses and autoimmunity. Cell-intrinsic canonical Notch signaling impaired T(reg) cell fitness and promoted the acquisition by T(reg) cells of a T(H)1 cell-like phenotype, whereas non-canonical Notch signaling dependent on the adaptor Rictor activated the kinase AKT-transcription factor Foxo1 axis and impaired the epigenetic stability of Foxp3. Our findings establish a critical role for Notch signaling in controlling peripheral T(reg) cell function.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Charbonnier</LastName>
<ForeName>Louis-Marie</ForeName>
<Initials>LM</Initials>
<AffiliationInfo><Affiliation>Division of Immunology, Boston Children's Hospital, Department of Pediatrics, Harvard Medical School, Boston, Massachusetts, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wang</LastName>
<ForeName>Sen</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Division of Immunology, Boston Children's Hospital, Department of Pediatrics, Harvard Medical School, Boston, Massachusetts, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Georgiev</LastName>
<ForeName>Peter</ForeName>
<Initials>P</Initials>
<AffiliationInfo><Affiliation>Division of Immunology, Boston Children's Hospital, Department of Pediatrics, Harvard Medical School, Boston, Massachusetts, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Sefik</LastName>
<ForeName>Esen</ForeName>
<Initials>E</Initials>
<AffiliationInfo><Affiliation>Division of Immunology, Department of Microbiology and Immunobiology, Harvard Medical School, Boston, Massachusetts, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Chatila</LastName>
<ForeName>Talal A</ForeName>
<Initials>TA</Initials>
<AffiliationInfo><Affiliation>Division of Immunology, Boston Children's Hospital, Department of Pediatrics, Harvard Medical School, Boston, Massachusetts, USA.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><GrantID>R01 AI085090</GrantID>
<Acronym>AI</Acronym>
<Agency>NIAID NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R56 AI115699</GrantID>
<Acronym>AI</Acronym>
<Agency>NIAID NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R01 AI065617</GrantID>
<Acronym>AI</Acronym>
<Agency>NIAID NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>2R01AI065617</GrantID>
<Acronym>AI</Acronym>
<Agency>NIAID NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>2R01AI085090</GrantID>
<Acronym>AI</Acronym>
<Agency>NIAID NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>1R56AI115699-01</GrantID>
<Acronym>AI</Acronym>
<Agency>NIAID 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>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2015</Year>
<Month>10</Month>
<Day>05</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>United States</Country>
<MedlineTA>Nat Immunol</MedlineTA>
<NlmUniqueID>100941354</NlmUniqueID>
<ISSNLinking>1529-2908</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D002352">Carrier Proteins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D051858">Forkhead Transcription Factors</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C498833">Foxp3 protein, mouse</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C497762">Notch1 protein, mouse</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000076226">Rapamycin-Insensitive Companion of mTOR Protein</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D051881">Receptor, Notch1</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D011993">Recombinant Fusion Proteins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C525637">rictor protein, mouse</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002352" MajorTopicYN="N">Carrier Proteins</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D044127" MajorTopicYN="N">Epigenesis, Genetic</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051858" MajorTopicYN="N">Forkhead Transcription Factors</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006086" MajorTopicYN="N">Graft vs Host Disease</DescriptorName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
<QualifierName UI="Q000517" MajorTopicYN="N">prevention & control</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008807" MajorTopicYN="N">Mice, Inbred BALB C</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018345" MajorTopicYN="N">Mice, Knockout</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008822" MajorTopicYN="N">Mice, Transgenic</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D009154" MajorTopicYN="N">Mutation</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D061166" MajorTopicYN="Y">Peripheral Tolerance</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000076226" MajorTopicYN="N">Rapamycin-Insensitive Companion of mTOR Protein</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051881" MajorTopicYN="N">Receptor, Notch1</DescriptorName>
<QualifierName UI="Q000172" MajorTopicYN="N">deficiency</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D011993" MajorTopicYN="N">Recombinant Fusion Proteins</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D050378" MajorTopicYN="N">T-Lymphocytes, Regulatory</DescriptorName>
<QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018417" MajorTopicYN="N">Th1 Cells</DescriptorName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D059467" MajorTopicYN="N">Transcriptome</DescriptorName>
</MeshHeading>
</MeshHeadingList>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2015</Year>
<Month>06</Month>
<Day>11</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted"><Year>2015</Year>
<Month>09</Month>
<Day>02</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="entrez"><Year>2015</Year>
<Month>10</Month>
<Day>6</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="pubmed"><Year>2015</Year>
<Month>10</Month>
<Day>6</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="medline"><Year>2016</Year>
<Month>4</Month>
<Day>23</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
</History>
<PublicationStatus>ppublish</PublicationStatus>
<ArticleIdList><ArticleId IdType="pubmed">26437242</ArticleId>
<ArticleId IdType="pii">ni.3288</ArticleId>
<ArticleId IdType="doi">10.1038/ni.3288</ArticleId>
<ArticleId IdType="pmc">PMC4618075</ArticleId>
<ArticleId IdType="mid">NIHMS720752</ArticleId>
</ArticleIdList>
<ReferenceList><Reference><Citation>Immunity. 2010 Dec 14;33(6):890-904</Citation>
<ArticleIdList><ArticleId IdType="pubmed">21167754</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Circulation. 2011 Jan 25;123(3):309-18</Citation>
<ArticleIdList><ArticleId IdType="pubmed">21220737</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Immunol. 2011 Jun 1;186(11):6199-206</Citation>
<ArticleIdList><ArticleId IdType="pubmed">21508258</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Immunol. 2011 Jul 15;187(2):692-701</Citation>
<ArticleIdList><ArticleId IdType="pubmed">21685328</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Biochim Biophys Acta. 2011 Nov;1813(11):1961-4</Citation>
<ArticleIdList><ArticleId IdType="pubmed">21238503</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Exp Med. 2012 Apr 9;209(4):713-28</Citation>
<ArticleIdList><ArticleId IdType="pubmed">22473959</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Annu Rev Immunol. 2010;28:343-65</Citation>
<ArticleIdList><ArticleId IdType="pubmed">20192807</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Int Immunol. 2006 Aug;18(8):1197-209</Citation>
<ArticleIdList><ArticleId IdType="pubmed">16772372</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Clin Exp Immunol. 2007 Jan;147(1):60-70</Citation>
<ArticleIdList><ArticleId IdType="pubmed">17177964</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>PLoS Biol. 2007 Feb;5(2):e38</Citation>
<ArticleIdList><ArticleId IdType="pubmed">17298177</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Nature. 2007 Feb 22;445(7130):931-5</Citation>
<ArticleIdList><ArticleId IdType="pubmed">17237765</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Immunity. 2007 Jul;27(1):100-10</Citation>
<ArticleIdList><ArticleId IdType="pubmed">17658278</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Immunity. 2007 Jul;27(1):89-99</Citation>
<ArticleIdList><ArticleId IdType="pubmed">17658279</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Immunity. 2007 Nov;27(5):786-800</Citation>
<ArticleIdList><ArticleId IdType="pubmed">18024188</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Lab Invest. 2008 Jan;88(1):11-7</Citation>
<ArticleIdList><ArticleId IdType="pubmed">18059366</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Immunity. 2008 Apr;28(4):546-58</Citation>
<ArticleIdList><ArticleId IdType="pubmed">18387831</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Blood. 2008 Sep 1;112(5):1813-21</Citation>
<ArticleIdList><ArticleId IdType="pubmed">18550850</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Nat Immunol. 2008 Oct;9(10):1140-7</Citation>
<ArticleIdList><ArticleId IdType="pubmed">18724371</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Curr Opin Genet Dev. 2008 Oct;18(5):449-54</Citation>
<ArticleIdList><ArticleId IdType="pubmed">18722525</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Mol Cell Biochem. 2009 Jan;320(1-2):109-14</Citation>
<ArticleIdList><ArticleId IdType="pubmed">18777163</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Nat Rev Immunol. 2009 Feb;9(2):116-24</Citation>
<ArticleIdList><ArticleId IdType="pubmed">19165228</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Immunol. 2009 Mar 15;182(6):3380-9</Citation>
<ArticleIdList><ArticleId IdType="pubmed">19265115</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Immunity. 2009 Mar 20;30(3):358-71</Citation>
<ArticleIdList><ArticleId IdType="pubmed">19285438</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cell Death Differ. 2009 Jun;16(6):879-89</Citation>
<ArticleIdList><ArticleId IdType="pubmed">19265851</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Nat Immunol. 2009 Jun;10(6):595-602</Citation>
<ArticleIdList><ArticleId IdType="pubmed">19412181</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Immunol. 2009 Jun 15;182(12):7381-8</Citation>
<ArticleIdList><ArticleId IdType="pubmed">19494260</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Nat Immunol. 2009 Sep;10(9):1000-7</Citation>
<ArticleIdList><ArticleId IdType="pubmed">19633673</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Immunity. 2009 Nov 20;31(5):772-86</Citation>
<ArticleIdList><ArticleId IdType="pubmed">19896394</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Nature. 2010 Feb 11;463(7282):808-12</Citation>
<ArticleIdList><ArticleId IdType="pubmed">20072126</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Int Immunol. 2002 Jun;14(6):637-45</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12039915</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Biol Chem. 2003 Apr 4;278(14):12361-6</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12517744</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Proc Natl Acad Sci U S A. 2003 Apr 29;100(9):5234-9</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12697902</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Immunity. 2003 Oct;19(4):549-59</Citation>
<ArticleIdList><ArticleId IdType="pubmed">14563319</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Proc Natl Acad Sci U S A. 2003 Dec 9;100(25):14920-5</Citation>
<ArticleIdList><ArticleId IdType="pubmed">14657333</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Immunol. 2012 Dec 15;189(12):5638-48</Citation>
<ArticleIdList><ArticleId IdType="pubmed">23125413</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Clin Invest. 2013 Apr;123(4):1590-604</Citation>
<ArticleIdList><ArticleId IdType="pubmed">23454750</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Immunol. 2013 Jun 1;190(11):5818-28</Citation>
<ArticleIdList><ArticleId IdType="pubmed">23636056</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Immunol. 2013 Jul 1;191(1):187-99</Citation>
<ArticleIdList><ArticleId IdType="pubmed">23733882</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Exp Med. 2013 Jul 1;210(7):1311-29</Citation>
<ArticleIdList><ArticleId IdType="pubmed">23733784</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Immunity. 2013 Jul 25;39(1):148-59</Citation>
<ArticleIdList><ArticleId IdType="pubmed">23890069</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Immunity. 2012 Apr 20;36(4):623-34</Citation>
<ArticleIdList><ArticleId IdType="pubmed">22503540</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Sci Signal. 2012 Jul 24;5(234):ra53</Citation>
<ArticleIdList><ArticleId IdType="pubmed">22827997</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Immunity. 2012 Sep 21;37(3):501-10</Citation>
<ArticleIdList><ArticleId IdType="pubmed">22960221</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Immunity. 2012 Nov 16;37(5):785-99</Citation>
<ArticleIdList><ArticleId IdType="pubmed">23123060</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Nature. 2012 Nov 22;491(7425):554-9</Citation>
<ArticleIdList><ArticleId IdType="pubmed">23135404</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Dev Biol. 2004 May 1;269(1):81-94</Citation>
<ArticleIdList><ArticleId IdType="pubmed">15081359</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cell. 2004 May 14;117(4):515-26</Citation>
<ArticleIdList><ArticleId IdType="pubmed">15137944</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Nat Immunol. 2005 Jul;6(7):680-8</Citation>
<ArticleIdList><ArticleId IdType="pubmed">15991363</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Exp Med. 2005 Oct 17;202(8):1037-42</Citation>
<ArticleIdList><ArticleId IdType="pubmed">16230473</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Proc Natl Acad Sci U S A. 2010 Mar 30;107(13):5919-24</Citation>
<ArticleIdList><ArticleId IdType="pubmed">20231436</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Immunity. 2010 Jan 29;32(1):14-27</Citation>
<ArticleIdList><ArticleId IdType="pubmed">20152168</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Immunity. 2015 Mar 17;42(3):512-23</Citation>
<ArticleIdList><ArticleId IdType="pubmed">25769611</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
</PubmedData>
</pubmed>
<affiliations><list><country><li>États-Unis</li>
</country>
<region><li>Massachusetts</li>
</region>
</list>
<tree><country name="États-Unis"><region name="Massachusetts"><name sortKey="Charbonnier, Louis Marie" sort="Charbonnier, Louis Marie" uniqKey="Charbonnier L" first="Louis-Marie" last="Charbonnier">Louis-Marie Charbonnier</name>
</region>
<name sortKey="Chatila, Talal A" sort="Chatila, Talal A" uniqKey="Chatila T" first="Talal A" last="Chatila">Talal A. Chatila</name>
<name sortKey="Georgiev, Peter" sort="Georgiev, Peter" uniqKey="Georgiev P" first="Peter" last="Georgiev">Peter Georgiev</name>
<name sortKey="Sefik, Esen" sort="Sefik, Esen" uniqKey="Sefik E" first="Esen" last="Sefik">Esen Sefik</name>
<name sortKey="Wang, Sen" sort="Wang, Sen" uniqKey="Wang S" first="Sen" last="Wang">Sen Wang</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 000D24 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd -nk 000D24 | 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:26437242 |texte= Control of peripheral tolerance by regulatory T cell-intrinsic Notch signaling. }}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Exploration/RBID.i -Sk "pubmed:26437242" \ | HfdSelect -Kh $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd \ | NlmPubMed2Wicri -a RapamycinFungusV1
This area was generated with Dilib version V0.6.38. |