RapamycinFungusV1, Main, Exploration, bibRecord, 000937

A population of innate myelolymphoblastoid effector cell expanded by inactivation of mTOR complex 1 in mice.

Identifieur interne : 000937 ( Main/Exploration ); précédent : 000936; suivant : 000938

A population of innate myelolymphoblastoid effector cell expanded by inactivation of mTOR complex 1 in mice.

Auteurs : Fei Tang [États-Unis] ; Peng Zhang [États-Unis, République populaire de Chine] ; Peiying Ye [États-Unis] ; Christopher A. Lazarski [États-Unis] ; Qi Wu [États-Unis] ; Ingrid L. Bergin [États-Unis] ; Timothy P. Bender [États-Unis] ; Michael N. Hall [Suisse] ; Ya Cui [République populaire de Chine] ; Liguo Zhang [République populaire de Chine] ; Taijiao Jiang [République populaire de Chine] ; Yang Liu [États-Unis] ; Pan Zheng [États-Unis]

Source :

eLife [ 2050-084X ] ; 2017.

RBID : pubmed:29206103

Descripteurs français

KwdFr :
- Animaux (MeSH), Antigènes de surface (analyse), Auto-immunité (MeSH), Complexe-1 cible mécanistique de la rapamycine (antagonistes et inhibiteurs), Délétion de gène (MeSH), Immunité innée (MeSH), Immunophénotypage (MeSH), Prolifération cellulaire (MeSH), Protéine de régulation associée à mTOR (génétique), Souris (MeSH), Sous-populations de lymphocytes (physiologie).
MESH :
- analyse : Antigènes de surface.
- antagonistes et inhibiteurs : Complexe-1 cible mécanistique de la rapamycine.
- génétique : Protéine de régulation associée à mTOR.
- physiologie : Sous-populations de lymphocytes.
- Animaux, Auto-immunité, Délétion de gène, Immunité innée, Immunophénotypage, Prolifération cellulaire, Souris.

English descriptors

KwdEn :
- Animals (MeSH), Antigens, Surface (analysis), Autoimmunity (MeSH), Cell Proliferation (MeSH), Gene Deletion (MeSH), Immunity, Innate (MeSH), Immunophenotyping (MeSH), Lymphocyte Subsets (physiology), Mechanistic Target of Rapamycin Complex 1 (antagonists & inhibitors), Mice (MeSH), Regulatory-Associated Protein of mTOR (genetics).
MESH :
- chemical , analysis : Antigens, Surface.
- chemical , antagonists & inhibitors : Mechanistic Target of Rapamycin Complex 1.
- chemical , genetics : Regulatory-Associated Protein of mTOR.
- physiology : Lymphocyte Subsets.
- Animals, Autoimmunity, Cell Proliferation, Gene Deletion, Immunity, Innate, Immunophenotyping, Mice.

Abstract

Adaptive autoimmunity is restrained by controlling population sizes and pathogenicity of harmful clones, while innate destruction is controlled at effector phase. We report here that deletion of Rptor in mouse hematopoietic stem/progenitor cells causes self-destructive innate immunity by massively increasing the population of previously uncharacterized innate myelolymphoblastoid effector cells (IMLECs). Mouse IMLECs are CD3^-B220^-NK1.1^-Ter119^- CD11c^low/-CD115^-F4/80^low/-Gr-1^- CD11b⁺, but surprisingly express high levels of PD-L1. Although they morphologically resemble lymphocytes and actively produce transcripts from Immunoglobulin loci, IMLECs have non-rearranged Ig loci, are phenotypically distinguishable from all known lymphocytes, and have a gene signature that bridges lymphoid and myeloid leukocytes. Rptor deletion unleashes differentiation of IMLECs from common myeloid progenitor cells by reducing expression of Myb. Importantly, IMLECs broadly overexpress pattern-recognition receptors and their expansion causes systemic inflammation in response to Toll-like receptor ligands in mice. Our data unveil a novel leukocyte population and an unrecognized role of Raptor/mTORC1 in innate immune tolerance.

DOI: 10.7554/eLife.32497
PubMed: 29206103
PubMed Central: PMC5762159

Affiliations:

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

to stream Main, to step Corpus: 000660
to stream Main, to step Curation: 000660

Le document en format XML

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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term>
<term>Antigens, Surface (analysis)</term>
<term>Autoimmunity (MeSH)</term>
<term>Cell Proliferation (MeSH)</term>
<term>Gene Deletion (MeSH)</term>
<term>Immunity, Innate (MeSH)</term>
<term>Immunophenotyping (MeSH)</term>
<term>Lymphocyte Subsets (physiology)</term>
<term>Mechanistic Target of Rapamycin Complex 1 (antagonists & inhibitors)</term>
<term>Mice (MeSH)</term>
<term>Regulatory-Associated Protein of mTOR (genetics)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term>
<term>Antigènes de surface (analyse)</term>
<term>Auto-immunité (MeSH)</term>
<term>Complexe-1 cible mécanistique de la rapamycine (antagonistes et inhibiteurs)</term>
<term>Délétion de gène (MeSH)</term>
<term>Immunité innée (MeSH)</term>
<term>Immunophénotypage (MeSH)</term>
<term>Prolifération cellulaire (MeSH)</term>
<term>Protéine de régulation associée à mTOR (génétique)</term>
<term>Souris (MeSH)</term>
<term>Sous-populations de lymphocytes (physiologie)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="analysis" xml:lang="en"><term>Antigens, Surface</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Mechanistic Target of Rapamycin Complex 1</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Regulatory-Associated Protein of mTOR</term>
</keywords>
<keywords scheme="MESH" qualifier="analyse" xml:lang="fr"><term>Antigènes de surface</term>
</keywords>
<keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Complexe-1 cible mécanistique de la rapamycine</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Protéine de régulation associée à mTOR</term>
</keywords>
<keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Sous-populations de lymphocytes</term>
</keywords>
<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Lymphocyte Subsets</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Autoimmunity</term>
<term>Cell Proliferation</term>
<term>Gene Deletion</term>
<term>Immunity, Innate</term>
<term>Immunophenotyping</term>
<term>Mice</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Auto-immunité</term>
<term>Délétion de gène</term>
<term>Immunité innée</term>
<term>Immunophénotypage</term>
<term>Prolifération cellulaire</term>
<term>Souris</term>
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<front><div type="abstract" xml:lang="en">Adaptive autoimmunity is restrained by controlling population sizes and pathogenicity of harmful clones, while innate destruction is controlled at effector phase. We report here that deletion of <i>Rptor</i>
 in mouse hematopoietic stem/progenitor cells causes self-destructive innate immunity by massively increasing the population of previously uncharacterized innate myelolymphoblastoid effector cells (IMLECs). Mouse IMLECs are CD3<sup>-</sup>
B220<sup>-</sup>
NK1.1<sup>-</sup>
Ter119<sup>-</sup>
 CD11c<sup>low/-</sup>
CD115<sup>-</sup>
F4/80<sup>low/-</sup>
Gr-1<sup>-</sup>
 CD11b<sup>+</sup>
, but surprisingly express high levels of PD-L1. Although they morphologically resemble lymphocytes and actively produce transcripts from Immunoglobulin loci, IMLECs have non-rearranged <i>Ig</i>
 loci, are phenotypically distinguishable from all known lymphocytes, and have a gene signature that bridges lymphoid and myeloid leukocytes. <i>Rptor</i>
 deletion unleashes differentiation of IMLECs from common myeloid progenitor cells by reducing expression of <i>Myb</i>
. Importantly, IMLECs broadly overexpress pattern-recognition receptors and their expansion causes systemic inflammation in response to Toll-like receptor ligands in mice. Our data unveil a novel leukocyte population and an unrecognized role of Raptor/mTORC1 in innate immune tolerance.</div>
</front>
</TEI>
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<Month>08</Month>
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<Day>13</Day>
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<Day>05</Day>
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<Title>eLife</Title>
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</Journal>
<ArticleTitle>A population of innate myelolymphoblastoid effector cell expanded by inactivation of mTOR complex 1 in mice.</ArticleTitle>
<ELocationID EIdType="doi" ValidYN="Y">10.7554/eLife.32497</ELocationID>
<ELocationID EIdType="pii" ValidYN="Y">e32497</ELocationID>
<Abstract><AbstractText>Adaptive autoimmunity is restrained by controlling population sizes and pathogenicity of harmful clones, while innate destruction is controlled at effector phase. We report here that deletion of <i>Rptor</i>
 in mouse hematopoietic stem/progenitor cells causes self-destructive innate immunity by massively increasing the population of previously uncharacterized innate myelolymphoblastoid effector cells (IMLECs). Mouse IMLECs are CD3<sup>-</sup>
B220<sup>-</sup>
NK1.1<sup>-</sup>
Ter119<sup>-</sup>
 CD11c<sup>low/-</sup>
CD115<sup>-</sup>
F4/80<sup>low/-</sup>
Gr-1<sup>-</sup>
 CD11b<sup>+</sup>
, but surprisingly express high levels of PD-L1. Although they morphologically resemble lymphocytes and actively produce transcripts from Immunoglobulin loci, IMLECs have non-rearranged <i>Ig</i>
 loci, are phenotypically distinguishable from all known lymphocytes, and have a gene signature that bridges lymphoid and myeloid leukocytes. <i>Rptor</i>
 deletion unleashes differentiation of IMLECs from common myeloid progenitor cells by reducing expression of <i>Myb</i>
. Importantly, IMLECs broadly overexpress pattern-recognition receptors and their expansion causes systemic inflammation in response to Toll-like receptor ligands in mice. Our data unveil a novel leukocyte population and an unrecognized role of Raptor/mTORC1 in innate immune tolerance.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Tang</LastName>
<ForeName>Fei</ForeName>
<Initials>F</Initials>
<Identifier Source="ORCID">http://orcid.org/0000-0003-1475-5028</Identifier>
<AffiliationInfo><Affiliation>Center for Cancer and Immunology Research, Children's Research Institute, Children's National Medical Center, Washington, United States.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zhang</LastName>
<ForeName>Peng</ForeName>
<Initials>P</Initials>
<Identifier Source="ORCID">http://orcid.org/0000-0002-6218-1885</Identifier>
<AffiliationInfo><Affiliation>Center for Cancer and Immunology Research, Children's Research Institute, Children's National Medical Center, Washington, United States.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Key Laboratory of Protein and Peptide Pharmaceuticals, Institute of Biophysics, Chinese Academy of Sciences, Beijing, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Ye</LastName>
<ForeName>Peiying</ForeName>
<Initials>P</Initials>
<AffiliationInfo><Affiliation>Center for Cancer and Immunology Research, Children's Research Institute, Children's National Medical Center, Washington, United States.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Lazarski</LastName>
<ForeName>Christopher A</ForeName>
<Initials>CA</Initials>
<AffiliationInfo><Affiliation>Center for Cancer and Immunology Research, Children's Research Institute, Children's National Medical Center, Washington, United States.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wu</LastName>
<ForeName>Qi</ForeName>
<Initials>Q</Initials>
<AffiliationInfo><Affiliation>Department of Neurology, University of Michigan Medical School, Ann Arbor, United States.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Bergin</LastName>
<ForeName>Ingrid L</ForeName>
<Initials>IL</Initials>
<AffiliationInfo><Affiliation>ULAM In-Vivo Animal Core, University of Michigan Medical School, Ann Arbor, United States.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Bender</LastName>
<ForeName>Timothy P</ForeName>
<Initials>TP</Initials>
<AffiliationInfo><Affiliation>Department of Microbiology, Immunology and Cancer Biology, University of Virginia, Charlottesville, United States.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Hall</LastName>
<ForeName>Michael N</ForeName>
<Initials>MN</Initials>
<AffiliationInfo><Affiliation>Biozentrum, University of Basel, Basel, Switzerland.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Cui</LastName>
<ForeName>Ya</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Key Laboratory of Protein and Peptide Pharmaceuticals, Institute of Biophysics, Chinese Academy of Sciences, Beijing, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zhang</LastName>
<ForeName>Liguo</ForeName>
<Initials>L</Initials>
<AffiliationInfo><Affiliation>Key Laboratory of Infection and Immunity, Institute of Biophysics, Chinese Academy of Sciences, Beijing, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Jiang</LastName>
<ForeName>Taijiao</ForeName>
<Initials>T</Initials>
<AffiliationInfo><Affiliation>Key Laboratory of Protein and Peptide Pharmaceuticals, Institute of Biophysics, Chinese Academy of Sciences, Beijing, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Liu</LastName>
<ForeName>Yang</ForeName>
<Initials>Y</Initials>
<Identifier Source="ORCID">http://orcid.org/0000-0002-9442-700X</Identifier>
<AffiliationInfo><Affiliation>Center for Cancer and Immunology Research, Children's Research Institute, Children's National Medical Center, Washington, United States.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zheng</LastName>
<ForeName>Pan</ForeName>
<Initials>P</Initials>
<Identifier Source="ORCID">http://orcid.org/0000-0003-2598-3544</Identifier>
<AffiliationInfo><Affiliation>Center for Cancer and Immunology Research, Children's Research Institute, Children's National Medical Center, Washington, United States.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><GrantID>U01 CA183030</GrantID>
<Acronym>CA</Acronym>
<Agency>NCI NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R01 AI064350</GrantID>
<Acronym>AI</Acronym>
<Agency>NIAID NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R01 AG036690</GrantID>
<Acronym>AG</Acronym>
<Agency>NIA NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R01 CA171972</GrantID>
<Acronym>CA</Acronym>
<Agency>NCI NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R01 GM100776</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>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2017</Year>
<Month>12</Month>
<Day>05</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>England</Country>
<MedlineTA>Elife</MedlineTA>
<NlmUniqueID>101579614</NlmUniqueID>
<ISSNLinking>2050-084X</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000954">Antigens, Surface</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000076223">Regulatory-Associated Protein of mTOR</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C540162">Rptor protein, mouse</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber>
<NameOfSubstance UI="D000076222">Mechanistic Target of Rapamycin Complex 1</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000954" MajorTopicYN="N">Antigens, Surface</DescriptorName>
<QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015551" MajorTopicYN="Y">Autoimmunity</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D049109" MajorTopicYN="Y">Cell Proliferation</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D017353" MajorTopicYN="N">Gene Deletion</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D007113" MajorTopicYN="Y">Immunity, Innate</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D016130" MajorTopicYN="N">Immunophenotyping</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D016131" MajorTopicYN="N">Lymphocyte Subsets</DescriptorName>
<QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000076222" MajorTopicYN="N">Mechanistic Target of Rapamycin Complex 1</DescriptorName>
<QualifierName UI="Q000037" MajorTopicYN="Y">antagonists & inhibitors</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000076223" MajorTopicYN="N">Regulatory-Associated Protein of mTOR</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">TSC-mTOR signaling</Keyword>
<Keyword MajorTopicYN="Y">hemotopoiesis</Keyword>
<Keyword MajorTopicYN="Y">immune tolerance</Keyword>
<Keyword MajorTopicYN="Y">immunology</Keyword>
<Keyword MajorTopicYN="Y">inflammation</Keyword>
<Keyword MajorTopicYN="Y">innate immunity</Keyword>
<Keyword MajorTopicYN="Y">mTORC1</Keyword>
<Keyword MajorTopicYN="Y">mouse</Keyword>
</KeywordList>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2017</Year>
<Month>10</Month>
<Day>03</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted"><Year>2017</Year>
<Month>12</Month>
<Day>02</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="pubmed"><Year>2017</Year>
<Month>12</Month>
<Day>6</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="medline"><Year>2018</Year>
<Month>8</Month>
<Day>23</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="entrez"><Year>2017</Year>
<Month>12</Month>
<Day>6</Day>
<Hour>6</Hour>
<Minute>0</Minute>
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</History>
<PublicationStatus>epublish</PublicationStatus>
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<affiliations><list><country><li>République populaire de Chine</li>
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A population of innate myelolymphoblastoid effector cell expanded by inactivation of mTOR complex 1 in mice.

A population of innate myelolymphoblastoid effector cell expanded by inactivation of mTOR complex 1 in mice.

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