mTORC2 signalling regulates M2 macrophage differentiation in response to helminth infection and adaptive thermogenesis.
Identifieur interne : 000682 ( Main/Exploration ); précédent : 000681; suivant : 000683mTORC2 signalling regulates M2 macrophage differentiation in response to helminth infection and adaptive thermogenesis.
Auteurs : R W Hallowell [États-Unis] ; S L Collins [États-Unis] ; J M Craig [États-Unis] ; Y. Zhang [République populaire de Chine] ; M. Oh [États-Unis] ; P B Illei [États-Unis] ; Y. Chan-Li [États-Unis] ; C L Vigeland [États-Unis] ; W. Mitzner [États-Unis] ; A L Scott [États-Unis] ; J D Powell [États-Unis] ; M R Horton [États-Unis]Source :
- Nature communications [ 2041-1723 ] ; 2017.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Cellules cultivées (MeSH), Compagnon de mTOR insensible à la rapamycine (génétique), Compagnon de mTOR insensible à la rapamycine (immunologie), Compagnon de mTOR insensible à la rapamycine (métabolisme), Complexe-2 cible mécanistique de la rapamycine (génétique), Complexe-2 cible mécanistique de la rapamycine (immunologie), Complexe-2 cible mécanistique de la rapamycine (métabolisme), Différenciation cellulaire (immunologie), Femelle (MeSH), Helminthoses animales (immunologie), Humains (MeSH), Immunité innée (physiologie), Infections à Strongylida (immunologie), Infections à Strongylida (parasitologie), Macrophages (physiologie), Modèles animaux de maladie humaine (MeSH), Mâle (MeSH), Nippostrongylus (immunologie), Souris (MeSH), Souris de lignée C57BL (MeSH), Techniques de knock-out de gènes (MeSH), Thermogenèse (physiologie), Transduction du signal (physiologie).
- MESH :
- génétique : Compagnon de mTOR insensible à la rapamycine, Complexe-2 cible mécanistique de la rapamycine.
- immunologie : Compagnon de mTOR insensible à la rapamycine, Complexe-2 cible mécanistique de la rapamycine, Différenciation cellulaire, Helminthoses animales, Infections à Strongylida, Nippostrongylus.
- métabolisme : Compagnon de mTOR insensible à la rapamycine, Complexe-2 cible mécanistique de la rapamycine.
- parasitologie : Infections à Strongylida.
- physiologie : Immunité innée, Macrophages, Thermogenèse, Transduction du signal.
- Animaux, Cellules cultivées, Femelle, Humains, Modèles animaux de maladie humaine, Mâle, Souris, Souris de lignée C57BL, Techniques de knock-out de gènes.
English descriptors
- KwdEn :
- Animals (MeSH), Cell Differentiation (immunology), Cells, Cultured (MeSH), Disease Models, Animal (MeSH), Female (MeSH), Gene Knockout Techniques (MeSH), Helminthiasis, Animal (immunology), Humans (MeSH), Immunity, Innate (physiology), Macrophages (physiology), Male (MeSH), Mechanistic Target of Rapamycin Complex 2 (genetics), Mechanistic Target of Rapamycin Complex 2 (immunology), Mechanistic Target of Rapamycin Complex 2 (metabolism), Mice (MeSH), Mice, Inbred C57BL (MeSH), Nippostrongylus (immunology), Rapamycin-Insensitive Companion of mTOR Protein (genetics), Rapamycin-Insensitive Companion of mTOR Protein (immunology), Rapamycin-Insensitive Companion of mTOR Protein (metabolism), Signal Transduction (physiology), Strongylida Infections (immunology), Strongylida Infections (parasitology), Thermogenesis (physiology).
- MESH :
- chemical , genetics : Mechanistic Target of Rapamycin Complex 2, Rapamycin-Insensitive Companion of mTOR Protein.
- immunology : Cell Differentiation, Helminthiasis, Animal, Mechanistic Target of Rapamycin Complex 2, Nippostrongylus, Rapamycin-Insensitive Companion of mTOR Protein, Strongylida Infections.
- chemical , metabolism : Mechanistic Target of Rapamycin Complex 2, Rapamycin-Insensitive Companion of mTOR Protein.
- parasitology : Strongylida Infections.
- physiology : Immunity, Innate, Macrophages, Signal Transduction, Thermogenesis.
- Animals, Cells, Cultured, Disease Models, Animal, Female, Gene Knockout Techniques, Humans, Male, Mice, Mice, Inbred C57BL.
Abstract
Alternatively activated macrophages (M2) have an important function in innate immune responses to parasitic helminths, and emerging evidence also indicates these cells are regulators of systemic metabolism. Here we show a critical role for mTORC2 signalling in the generation of M2 macrophages. Abrogation of mTORC2 signalling in macrophages by selective conditional deletion of the adaptor molecule Rictor inhibits the generation of M2 macrophages while leaving the generation of classically activated macrophages (M1) intact. Selective deletion of Rictor in macrophages prevents M2 differentiation and clearance of a parasitic helminth infection in mice, and also abrogates the ability of mice to regulate brown fat and maintain core body temperature. Our findings define a role for mTORC2 in macrophages in integrating signals from the immune microenvironment to promote innate type 2 immunity, and also to integrate systemic metabolic and thermogenic responses.
DOI: 10.1038/ncomms14208
PubMed: 28128208
PubMed Central: PMC5290163
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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Zhang</name><affiliation wicri:level="1"><nlm:affiliation>Department of Respiratory Diseases, Shanghai Pulmonary Hospital, Tongji University School of Medicine, 1239 Siping Road, Shanghai 200433, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Respiratory Diseases, Shanghai Pulmonary Hospital, Tongji University School of Medicine, 1239 Siping Road, Shanghai 200433</wicri:regionArea><wicri:noRegion>Shanghai 200433</wicri:noRegion></affiliation></author><author><name sortKey="Oh, M" sort="Oh, M" uniqKey="Oh M" first="M" last="Oh">M. 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Mitzner</name><affiliation wicri:level="1"><nlm:affiliation>W. Harry Feinstone Department of Molecular Microbiology and Immunology, Bloomberg School of Public Health, Johns Hopkins University, 650 North Wolfe Street, Baltimore, Maryland 21205, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>W. Harry Feinstone Department of Molecular Microbiology and Immunology, Bloomberg School of Public Health, Johns Hopkins University, 650 North Wolfe Street, Baltimore, Maryland 21205</wicri:regionArea><wicri:noRegion>Maryland 21205</wicri:noRegion></affiliation></author><author><name sortKey="Scott, A L" sort="Scott, A L" uniqKey="Scott A" first="A L" last="Scott">A L Scott</name><affiliation wicri:level="1"><nlm:affiliation>W. Harry Feinstone Department of Molecular Microbiology and Immunology, Bloomberg School of Public Health, Johns Hopkins University, 650 North Wolfe Street, Baltimore, Maryland 21205, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>W. Harry Feinstone Department of Molecular Microbiology and Immunology, Bloomberg School of Public Health, Johns Hopkins University, 650 North Wolfe Street, Baltimore, Maryland 21205</wicri:regionArea><wicri:noRegion>Maryland 21205</wicri:noRegion></affiliation></author><author><name sortKey="Powell, J D" sort="Powell, J D" uniqKey="Powell J" first="J D" last="Powell">J D Powell</name><affiliation wicri:level="1"><nlm:affiliation>Department of Oncology, Johns Hopkins University School of Medicine, 735 North Broadway, Baltimore, Maryland 21205, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Oncology, Johns Hopkins University School of Medicine, 735 North Broadway, Baltimore, Maryland 21205</wicri:regionArea><wicri:noRegion>Maryland 21205</wicri:noRegion></affiliation></author><author><name sortKey="Horton, M R" sort="Horton, M R" uniqKey="Horton M" first="M R" last="Horton">M R Horton</name><affiliation wicri:level="1"><nlm:affiliation>Department of Medicine, Johns Hopkins University School of Medicine, 735 North Broadway, Baltimore, Maryland 21205, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Medicine, Johns Hopkins University School of Medicine, 735 North Broadway, Baltimore, Maryland 21205</wicri:regionArea><wicri:noRegion>Maryland 21205</wicri:noRegion></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2017">2017</date><idno type="RBID">pubmed:28128208</idno><idno type="pmid">28128208</idno><idno type="doi">10.1038/ncomms14208</idno><idno type="pmc">PMC5290163</idno><idno type="wicri:Area/Main/Corpus">000885</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000885</idno><idno type="wicri:Area/Main/Curation">000885</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Curation">000885</idno><idno type="wicri:Area/Main/Exploration">000885</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">mTORC2 signalling regulates M2 macrophage differentiation in response to helminth infection and adaptive thermogenesis.</title><author><name sortKey="Hallowell, R W" sort="Hallowell, R W" uniqKey="Hallowell R" first="R W" last="Hallowell">R W Hallowell</name><affiliation wicri:level="1"><nlm:affiliation>Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brooklyn Avenue, Boston, Massachusetts 02215, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brooklyn Avenue, Boston, Massachusetts 02215</wicri:regionArea><wicri:noRegion>Massachusetts 02215</wicri:noRegion></affiliation></author><author><name sortKey="Collins, S L" sort="Collins, S L" uniqKey="Collins S" first="S L" last="Collins">S L Collins</name><affiliation wicri:level="1"><nlm:affiliation>Department of Medicine, Johns Hopkins University School of Medicine, 735 North Broadway, Baltimore, Maryland 21205, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Medicine, Johns Hopkins University School of Medicine, 735 North Broadway, Baltimore, Maryland 21205</wicri:regionArea><wicri:noRegion>Maryland 21205</wicri:noRegion></affiliation></author><author><name sortKey="Craig, J M" sort="Craig, J M" uniqKey="Craig J" first="J M" last="Craig">J M Craig</name><affiliation wicri:level="1"><nlm:affiliation>Department of Environmental Health Sciences, Johns Hopkins Bloomberg School of Public Health, 650 North Wolfe Street, Baltimore, Maryland 21205, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Environmental Health Sciences, Johns Hopkins Bloomberg School of Public Health, 650 North Wolfe Street, Baltimore, Maryland 21205</wicri:regionArea><wicri:noRegion>Maryland 21205</wicri:noRegion></affiliation></author><author><name sortKey="Zhang, Y" sort="Zhang, Y" uniqKey="Zhang Y" first="Y" last="Zhang">Y. Zhang</name><affiliation wicri:level="1"><nlm:affiliation>Department of Respiratory Diseases, Shanghai Pulmonary Hospital, Tongji University School of Medicine, 1239 Siping Road, Shanghai 200433, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Respiratory Diseases, Shanghai Pulmonary Hospital, Tongji University School of Medicine, 1239 Siping Road, Shanghai 200433</wicri:regionArea><wicri:noRegion>Shanghai 200433</wicri:noRegion></affiliation></author><author><name sortKey="Oh, M" sort="Oh, M" uniqKey="Oh M" first="M" last="Oh">M. Oh</name><affiliation wicri:level="1"><nlm:affiliation>Department of Oncology, Johns Hopkins University School of Medicine, 735 North Broadway, Baltimore, Maryland 21205, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Oncology, Johns Hopkins University School of Medicine, 735 North Broadway, Baltimore, Maryland 21205</wicri:regionArea><wicri:noRegion>Maryland 21205</wicri:noRegion></affiliation></author><author><name sortKey="Illei, P B" sort="Illei, P B" uniqKey="Illei P" first="P B" last="Illei">P B Illei</name><affiliation wicri:level="1"><nlm:affiliation>Department of Pathology, Johns Hopkins University School of Medicine, 735 North Broadway, Baltimore, Maryland 21205, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pathology, Johns Hopkins University School of Medicine, 735 North Broadway, Baltimore, Maryland 21205</wicri:regionArea><wicri:noRegion>Maryland 21205</wicri:noRegion></affiliation></author><author><name sortKey="Chan Li, Y" sort="Chan Li, Y" uniqKey="Chan Li Y" first="Y" last="Chan-Li">Y. Chan-Li</name><affiliation wicri:level="1"><nlm:affiliation>Department of Medicine, Johns Hopkins University School of Medicine, 735 North Broadway, Baltimore, Maryland 21205, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Medicine, Johns Hopkins University School of Medicine, 735 North Broadway, Baltimore, Maryland 21205</wicri:regionArea><wicri:noRegion>Maryland 21205</wicri:noRegion></affiliation></author><author><name sortKey="Vigeland, C L" sort="Vigeland, C L" uniqKey="Vigeland C" first="C L" last="Vigeland">C L Vigeland</name><affiliation wicri:level="1"><nlm:affiliation>Department of Medicine, Johns Hopkins University School of Medicine, 735 North Broadway, Baltimore, Maryland 21205, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Medicine, Johns Hopkins University School of Medicine, 735 North Broadway, Baltimore, Maryland 21205</wicri:regionArea><wicri:noRegion>Maryland 21205</wicri:noRegion></affiliation></author><author><name sortKey="Mitzner, W" sort="Mitzner, W" uniqKey="Mitzner W" first="W" last="Mitzner">W. Mitzner</name><affiliation wicri:level="1"><nlm:affiliation>W. Harry Feinstone Department of Molecular Microbiology and Immunology, Bloomberg School of Public Health, Johns Hopkins University, 650 North Wolfe Street, Baltimore, Maryland 21205, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>W. Harry Feinstone Department of Molecular Microbiology and Immunology, Bloomberg School of Public Health, Johns Hopkins University, 650 North Wolfe Street, Baltimore, Maryland 21205</wicri:regionArea><wicri:noRegion>Maryland 21205</wicri:noRegion></affiliation></author><author><name sortKey="Scott, A L" sort="Scott, A L" uniqKey="Scott A" first="A L" last="Scott">A L Scott</name><affiliation wicri:level="1"><nlm:affiliation>W. Harry Feinstone Department of Molecular Microbiology and Immunology, Bloomberg School of Public Health, Johns Hopkins University, 650 North Wolfe Street, Baltimore, Maryland 21205, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>W. Harry Feinstone Department of Molecular Microbiology and Immunology, Bloomberg School of Public Health, Johns Hopkins University, 650 North Wolfe Street, Baltimore, Maryland 21205</wicri:regionArea><wicri:noRegion>Maryland 21205</wicri:noRegion></affiliation></author><author><name sortKey="Powell, J D" sort="Powell, J D" uniqKey="Powell J" first="J D" last="Powell">J D Powell</name><affiliation wicri:level="1"><nlm:affiliation>Department of Oncology, Johns Hopkins University School of Medicine, 735 North Broadway, Baltimore, Maryland 21205, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Oncology, Johns Hopkins University School of Medicine, 735 North Broadway, Baltimore, Maryland 21205</wicri:regionArea><wicri:noRegion>Maryland 21205</wicri:noRegion></affiliation></author><author><name sortKey="Horton, M R" sort="Horton, M R" uniqKey="Horton M" first="M R" last="Horton">M R Horton</name><affiliation wicri:level="1"><nlm:affiliation>Department of Medicine, Johns Hopkins University School of Medicine, 735 North Broadway, Baltimore, Maryland 21205, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Medicine, Johns Hopkins University School of Medicine, 735 North Broadway, Baltimore, Maryland 21205</wicri:regionArea><wicri:noRegion>Maryland 21205</wicri:noRegion></affiliation></author></analytic><series><title level="j">Nature communications</title><idno type="eISSN">2041-1723</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term><term>Cell Differentiation (immunology)</term><term>Cells, Cultured (MeSH)</term><term>Disease Models, Animal (MeSH)</term><term>Female (MeSH)</term><term>Gene Knockout Techniques (MeSH)</term><term>Helminthiasis, Animal (immunology)</term><term>Humans (MeSH)</term><term>Immunity, Innate (physiology)</term><term>Macrophages (physiology)</term><term>Male (MeSH)</term><term>Mechanistic Target of Rapamycin Complex 2 (genetics)</term><term>Mechanistic Target of Rapamycin Complex 2 (immunology)</term><term>Mechanistic Target of Rapamycin Complex 2 (metabolism)</term><term>Mice (MeSH)</term><term>Mice, Inbred C57BL (MeSH)</term><term>Nippostrongylus (immunology)</term><term>Rapamycin-Insensitive Companion of mTOR Protein (genetics)</term><term>Rapamycin-Insensitive Companion of mTOR Protein (immunology)</term><term>Rapamycin-Insensitive Companion of mTOR Protein (metabolism)</term><term>Signal Transduction (physiology)</term><term>Strongylida Infections (immunology)</term><term>Strongylida Infections (parasitology)</term><term>Thermogenesis (physiology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term><term>Cellules cultivées (MeSH)</term><term>Compagnon de mTOR insensible à la rapamycine (génétique)</term><term>Compagnon de mTOR insensible à la rapamycine (immunologie)</term><term>Compagnon de mTOR insensible à la rapamycine (métabolisme)</term><term>Complexe-2 cible mécanistique de la rapamycine (génétique)</term><term>Complexe-2 cible mécanistique de la rapamycine (immunologie)</term><term>Complexe-2 cible mécanistique de la rapamycine (métabolisme)</term><term>Différenciation cellulaire (immunologie)</term><term>Femelle (MeSH)</term><term>Helminthoses animales (immunologie)</term><term>Humains (MeSH)</term><term>Immunité innée (physiologie)</term><term>Infections à Strongylida (immunologie)</term><term>Infections à Strongylida (parasitologie)</term><term>Macrophages (physiologie)</term><term>Modèles animaux de maladie humaine (MeSH)</term><term>Mâle (MeSH)</term><term>Nippostrongylus (immunologie)</term><term>Souris (MeSH)</term><term>Souris de lignée C57BL (MeSH)</term><term>Techniques de knock-out de gènes (MeSH)</term><term>Thermogenèse (physiologie)</term><term>Transduction du signal (physiologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Mechanistic Target of Rapamycin Complex 2</term><term>Rapamycin-Insensitive Companion of mTOR Protein</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Compagnon de mTOR insensible à la rapamycine</term><term>Complexe-2 cible mécanistique de la rapamycine</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Compagnon de mTOR insensible à la rapamycine</term><term>Complexe-2 cible mécanistique de la rapamycine</term><term>Différenciation cellulaire</term><term>Helminthoses animales</term><term>Infections à Strongylida</term><term>Nippostrongylus</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Cell Differentiation</term><term>Helminthiasis, Animal</term><term>Mechanistic Target of Rapamycin Complex 2</term><term>Nippostrongylus</term><term>Rapamycin-Insensitive Companion of mTOR Protein</term><term>Strongylida Infections</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Mechanistic Target of Rapamycin Complex 2</term><term>Rapamycin-Insensitive Companion of mTOR Protein</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Compagnon de mTOR insensible à la rapamycine</term><term>Complexe-2 cible mécanistique de la rapamycine</term></keywords><keywords scheme="MESH" qualifier="parasitologie" xml:lang="fr"><term>Infections à Strongylida</term></keywords><keywords scheme="MESH" qualifier="parasitology" xml:lang="en"><term>Strongylida Infections</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Immunité innée</term><term>Macrophages</term><term>Thermogenèse</term><term>Transduction du signal</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Immunity, Innate</term><term>Macrophages</term><term>Signal Transduction</term><term>Thermogenesis</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cells, Cultured</term><term>Disease Models, Animal</term><term>Female</term><term>Gene Knockout Techniques</term><term>Humans</term><term>Male</term><term>Mice</term><term>Mice, Inbred C57BL</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Cellules cultivées</term><term>Femelle</term><term>Humains</term><term>Modèles animaux de maladie humaine</term><term>Mâle</term><term>Souris</term><term>Souris de lignée C57BL</term><term>Techniques de knock-out de gènes</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Alternatively activated macrophages (M2) have an important function in innate immune responses to parasitic helminths, and emerging evidence also indicates these cells are regulators of systemic metabolism. Here we show a critical role for mTORC2 signalling in the generation of M2 macrophages. Abrogation of mTORC2 signalling in macrophages by selective conditional deletion of the adaptor molecule Rictor inhibits the generation of M2 macrophages while leaving the generation of classically activated macrophages (M1) intact. Selective deletion of Rictor in macrophages prevents M2 differentiation and clearance of a parasitic helminth infection in mice, and also abrogates the ability of mice to regulate brown fat and maintain core body temperature. Our findings define a role for mTORC2 in macrophages in integrating signals from the immune microenvironment to promote innate type 2 immunity, and also to integrate systemic metabolic and thermogenic responses.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">28128208</PMID><DateCompleted><Year>2018</Year><Month>12</Month><Day>11</Day></DateCompleted><DateRevised><Year>2018</Year><Month>12</Month><Day>11</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">2041-1723</ISSN><JournalIssue CitedMedium="Internet"><Volume>8</Volume><PubDate><Year>2017</Year><Month>01</Month><Day>27</Day></PubDate></JournalIssue><Title>Nature communications</Title><ISOAbbreviation>Nat Commun</ISOAbbreviation></Journal><ArticleTitle>mTORC2 signalling regulates M2 macrophage differentiation in response to helminth infection and adaptive thermogenesis.</ArticleTitle><Pagination><MedlinePgn>14208</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1038/ncomms14208</ELocationID><Abstract><AbstractText>Alternatively activated macrophages (M2) have an important function in innate immune responses to parasitic helminths, and emerging evidence also indicates these cells are regulators of systemic metabolism. Here we show a critical role for mTORC2 signalling in the generation of M2 macrophages. Abrogation of mTORC2 signalling in macrophages by selective conditional deletion of the adaptor molecule Rictor inhibits the generation of M2 macrophages while leaving the generation of classically activated macrophages (M1) intact. Selective deletion of Rictor in macrophages prevents M2 differentiation and clearance of a parasitic helminth infection in mice, and also abrogates the ability of mice to regulate brown fat and maintain core body temperature. Our findings define a role for mTORC2 in macrophages in integrating signals from the immune microenvironment to promote innate type 2 immunity, and also to integrate systemic metabolic and thermogenic responses.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Hallowell</LastName><ForeName>R W</ForeName><Initials>RW</Initials><AffiliationInfo><Affiliation>Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brooklyn Avenue, Boston, Massachusetts 02215, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Collins</LastName><ForeName>S L</ForeName><Initials>SL</Initials><AffiliationInfo><Affiliation>Department of Medicine, Johns Hopkins University School of Medicine, 735 North Broadway, Baltimore, Maryland 21205, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Craig</LastName><ForeName>J M</ForeName><Initials>JM</Initials><AffiliationInfo><Affiliation>Department of Environmental Health Sciences, Johns Hopkins Bloomberg School of Public Health, 650 North Wolfe Street, Baltimore, Maryland 21205, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Y</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Respiratory Diseases, Shanghai Pulmonary Hospital, Tongji University School of Medicine, 1239 Siping Road, Shanghai 200433, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Oh</LastName><ForeName>M</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Oncology, Johns Hopkins University School of Medicine, 735 North Broadway, Baltimore, Maryland 21205, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Illei</LastName><ForeName>P B</ForeName><Initials>PB</Initials><AffiliationInfo><Affiliation>Department of Pathology, Johns Hopkins University School of Medicine, 735 North Broadway, Baltimore, Maryland 21205, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chan-Li</LastName><ForeName>Y</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Medicine, Johns Hopkins University School of Medicine, 735 North Broadway, Baltimore, Maryland 21205, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Vigeland</LastName><ForeName>C L</ForeName><Initials>CL</Initials><AffiliationInfo><Affiliation>Department of Medicine, Johns Hopkins University School of Medicine, 735 North Broadway, Baltimore, Maryland 21205, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mitzner</LastName><ForeName>W</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>W. Harry Feinstone Department of Molecular Microbiology and Immunology, Bloomberg School of Public Health, Johns Hopkins University, 650 North Wolfe Street, Baltimore, Maryland 21205, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Scott</LastName><ForeName>A L</ForeName><Initials>AL</Initials><AffiliationInfo><Affiliation>W. Harry Feinstone Department of Molecular Microbiology and Immunology, Bloomberg School of Public Health, Johns Hopkins University, 650 North Wolfe Street, Baltimore, Maryland 21205, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Powell</LastName><ForeName>J D</ForeName><Initials>JD</Initials><AffiliationInfo><Affiliation>Department of Oncology, Johns Hopkins University School of Medicine, 735 North Broadway, Baltimore, Maryland 21205, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Horton</LastName><ForeName>M R</ForeName><Initials>MR</Initials><AffiliationInfo><Affiliation>Department of Medicine, Johns Hopkins University School of Medicine, 735 North Broadway, Baltimore, Maryland 21205, USA.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>F32 HL124823</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P01 HL010342</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R21 HL111783</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>T32 AI007247</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><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2017</Year><Month>01</Month><Day>27</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Nat Commun</MedlineTA><NlmUniqueID>101528555</NlmUniqueID><ISSNLinking>2041-1723</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000076226">Rapamycin-Insensitive Companion of mTOR Protein</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C525637">rictor protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber><NameOfSubstance UI="D000076225">Mechanistic Target of Rapamycin Complex 2</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002454" MajorTopicYN="N">Cell Differentiation</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002478" MajorTopicYN="N">Cells, Cultured</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D055786" MajorTopicYN="N">Gene Knockout Techniques</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006374" MajorTopicYN="N">Helminthiasis, Animal</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007113" MajorTopicYN="N">Immunity, Innate</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008264" MajorTopicYN="N">Macrophages</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000076225" MajorTopicYN="N">Mechanistic Target of Rapamycin Complex 2</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">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="D009559" MajorTopicYN="N">Nippostrongylus</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000076226" MajorTopicYN="N">Rapamycin-Insensitive Companion of mTOR Protein</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017206" MajorTopicYN="N">Strongylida Infections</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000469" MajorTopicYN="N">parasitology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D022722" MajorTopicYN="N">Thermogenesis</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading></MeshHeadingList><CoiStatement>The authors declare no competing financial interests.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2016</Year><Month>03</Month><Day>18</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2016</Year><Month>12</Month><Day>05</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2017</Year><Month>1</Month><Day>28</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2017</Year><Month>1</Month><Day>28</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2018</Year><Month>12</Month><Day>12</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">28128208</ArticleId><ArticleId IdType="pii">ncomms14208</ArticleId><ArticleId IdType="doi">10.1038/ncomms14208</ArticleId><ArticleId IdType="pmc">PMC5290163</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Immunity. 2008 Oct 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Chan-Li</name><name sortKey="Collins, S L" sort="Collins, S L" uniqKey="Collins S" first="S L" last="Collins">S L Collins</name><name sortKey="Craig, J M" sort="Craig, J M" uniqKey="Craig J" first="J M" last="Craig">J M Craig</name><name sortKey="Horton, M R" sort="Horton, M R" uniqKey="Horton M" first="M R" last="Horton">M R Horton</name><name sortKey="Illei, P B" sort="Illei, P B" uniqKey="Illei P" first="P B" last="Illei">P B Illei</name><name sortKey="Mitzner, W" sort="Mitzner, W" uniqKey="Mitzner W" first="W" last="Mitzner">W. Mitzner</name><name sortKey="Oh, M" sort="Oh, M" uniqKey="Oh M" first="M" last="Oh">M. Oh</name><name sortKey="Powell, J D" sort="Powell, J D" uniqKey="Powell J" first="J D" last="Powell">J D Powell</name><name sortKey="Scott, A L" sort="Scott, A L" uniqKey="Scott A" first="A L" last="Scott">A L Scott</name><name sortKey="Vigeland, C L" sort="Vigeland, C L" uniqKey="Vigeland C" first="C L" last="Vigeland">C L Vigeland</name></country><country name="République populaire de Chine"><noRegion><name sortKey="Zhang, Y" sort="Zhang, Y" uniqKey="Zhang Y" first="Y" last="Zhang">Y. Zhang</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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