Tumor Microenvironment Modulates Immunological Outcomes of Myeloid Cells with mTORC1 Disruption.
Identifieur interne : 000185 ( Main/Exploration ); précédent : 000184; suivant : 000186Tumor Microenvironment Modulates Immunological Outcomes of Myeloid Cells with mTORC1 Disruption.
Auteurs : Chuanlin Ding [États-Unis] ; Xiaomin Sun [États-Unis] ; Caijun Wu [États-Unis] ; Xiaoling Hu [États-Unis] ; Huang-Ge Zhang [États-Unis] ; Jun Yan [États-Unis]Source :
- Journal of immunology (Baltimore, Md. : 1950) [ 1550-6606 ] ; 2019.
Descripteurs français
- KwdFr :
- MESH :
- anatomopathologie : Tumeurs du poumon.
- immunologie : Cellules myéloïdes, Complexe-1 cible mécanistique de la rapamycine, Microenvironnement tumoral, Tumeurs du poumon.
- Animaux, Souris, Souris knockout, Souris transgéniques.
English descriptors
- KwdEn :
- MESH :
- chemical , immunology : Mechanistic Target of Rapamycin Complex 1.
- immunology : Lung Neoplasms, Myeloid Cells, Tumor Microenvironment.
- pathology : Lung Neoplasms.
- Animals, Mice, Mice, Knockout, Mice, Transgenic.
Abstract
The role of the mTOR signaling pathway in different myeloid cell subsets is poorly understood in the context of tumor development. In this study, myeloid cell-specific Raptor knockout (KO) mice were used to determine the roles of mechanistic target of rapamycin complex 1 (mTORC1) in regulating macrophage function from Lewis lung carcinoma (LLC) s.c. tumors and lung tumor metastasis. We found no difference in tumor growth between conditional Raptor KO and control mice in the s.c. tumor models, although depletion of mTORC1 decreased the immunosuppressive function of tumor-associated macrophages (TAM). Despite the decreased immunosuppressive activity of TAM, M1-like TAM differentiation was impaired in the s.c. tumor microenvironment of mTORC1 conditional Raptor KO mice due to downregulated CD115 expression on macrophages. In addition, TNF-α production by mTORC1-deficient myeloid cells was also decreased in the s.c. LLC tumors. On the contrary, disruption of mTORC1 in myeloid cells promoted lung cancer metastasis. Accordingly, immunosuppressive interstitial macrophages/metastasis-associated macrophages (CD11b+F4/80high) were accumulated in the lungs of Raptor KO mice in the LLC lung metastasis model, leading to decreased Th1 responses. Taken together, our results demonstrate that differential tumor microenvironment dictates the immunological outcomes of myeloid cells, with mTORC1 disruption leading to different tumor growth phenotypes.
DOI: 10.4049/jimmunol.1801112
PubMed: 30665937
PubMed Central: PMC6382613
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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and Department of Microbiology and Immunology, James Graham Brown Cancer Center, University of Louisville, Louisville, KY 40202 chuanlin.ding@louisville.edu jun.yan@louisville.edu.</nlm:affiliation><country wicri:rule="url">États-Unis</country><wicri:regionArea>Department of Medicine, James Graham Brown Cancer Center, University of Louisville, Louisville, KY 40202; and Department of Microbiology and Immunology, James Graham Brown Cancer Center, University of Louisville, Louisville</wicri:regionArea><wicri:noRegion>Louisville</wicri:noRegion></affiliation></author><author><name sortKey="Sun, Xiaomin" sort="Sun, Xiaomin" uniqKey="Sun X" first="Xiaomin" last="Sun">Xiaomin Sun</name><affiliation wicri:level="2"><nlm:affiliation>Department of Medicine, James Graham Brown Cancer Center, University of Louisville, Louisville, KY 40202; and Department of Microbiology and Immunology, James Graham Brown Cancer Center, University of Louisville, Louisville, KY 40202.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Kentucky</region></placeName><wicri:cityArea>Department of Medicine, James Graham Brown Cancer Center, University of Louisville, Louisville, KY 40202; 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and Department of Microbiology and Immunology, James Graham Brown Cancer Center, University of Louisville, Louisville, KY 40202.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Kentucky</region></placeName><wicri:cityArea>Department of Medicine, James Graham Brown Cancer Center, University of Louisville, Louisville, KY 40202; and Department of Microbiology and Immunology, James Graham Brown Cancer Center, University of Louisville, Louisville</wicri:cityArea></affiliation></author><author><name sortKey="Zhang, Huang Ge" sort="Zhang, Huang Ge" uniqKey="Zhang H" first="Huang-Ge" last="Zhang">Huang-Ge Zhang</name><affiliation wicri:level="2"><nlm:affiliation>Department of Medicine, James Graham Brown Cancer Center, University of Louisville, Louisville, KY 40202; and Department of Microbiology and Immunology, James Graham Brown Cancer Center, University of Louisville, Louisville, KY 40202.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Kentucky</region></placeName><wicri:cityArea>Department of Medicine, James Graham Brown Cancer Center, University of Louisville, Louisville, KY 40202; and Department of Microbiology and Immunology, James Graham Brown Cancer Center, University of Louisville, Louisville</wicri:cityArea></affiliation></author><author><name sortKey="Yan, Jun" sort="Yan, Jun" uniqKey="Yan J" first="Jun" last="Yan">Jun Yan</name><affiliation wicri:level="1"><nlm:affiliation>Department of Medicine, James Graham Brown Cancer Center, University of Louisville, Louisville, KY 40202; and Department of Microbiology and Immunology, James Graham Brown Cancer Center, University of Louisville, Louisville, KY 40202 chuanlin.ding@louisville.edu jun.yan@louisville.edu.</nlm:affiliation><country wicri:rule="url">États-Unis</country><wicri:regionArea>Department of Medicine, James Graham Brown Cancer Center, University of Louisville, Louisville, KY 40202; and Department of Microbiology and Immunology, James Graham Brown Cancer Center, University of Louisville, Louisville</wicri:regionArea><wicri:noRegion>Louisville</wicri:noRegion></affiliation></author></analytic><series><title level="j">Journal of immunology (Baltimore, Md. : 1950)</title><idno type="eISSN">1550-6606</idno><imprint><date when="2019" type="published">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term><term>Lung Neoplasms (immunology)</term><term>Lung Neoplasms (pathology)</term><term>Mechanistic Target of Rapamycin Complex 1 (immunology)</term><term>Mice (MeSH)</term><term>Mice, Knockout (MeSH)</term><term>Mice, Transgenic (MeSH)</term><term>Myeloid Cells (immunology)</term><term>Tumor Microenvironment (immunology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term><term>Cellules myéloïdes (immunologie)</term><term>Complexe-1 cible mécanistique de la rapamycine (immunologie)</term><term>Microenvironnement tumoral (immunologie)</term><term>Souris (MeSH)</term><term>Souris knockout (MeSH)</term><term>Souris transgéniques (MeSH)</term><term>Tumeurs du poumon (anatomopathologie)</term><term>Tumeurs du poumon (immunologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Mechanistic Target of Rapamycin Complex 1</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Tumeurs du poumon</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Cellules myéloïdes</term><term>Complexe-1 cible mécanistique de la rapamycine</term><term>Microenvironnement tumoral</term><term>Tumeurs du poumon</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Lung Neoplasms</term><term>Myeloid Cells</term><term>Tumor Microenvironment</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Lung Neoplasms</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Mice</term><term>Mice, Knockout</term><term>Mice, Transgenic</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Souris</term><term>Souris knockout</term><term>Souris transgéniques</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The role of the mTOR signaling pathway in different myeloid cell subsets is poorly understood in the context of tumor development. In this study, myeloid cell-specific Raptor knockout (KO) mice were used to determine the roles of mechanistic target of rapamycin complex 1 (mTORC1) in regulating macrophage function from Lewis lung carcinoma (LLC) s.c. tumors and lung tumor metastasis. We found no difference in tumor growth between conditional Raptor KO and control mice in the s.c. tumor models, although depletion of mTORC1 decreased the immunosuppressive function of tumor-associated macrophages (TAM). Despite the decreased immunosuppressive activity of TAM, M1-like TAM differentiation was impaired in the s.c. tumor microenvironment of mTORC1 conditional Raptor KO mice due to downregulated CD115 expression on macrophages. In addition, TNF-α production by mTORC1-deficient myeloid cells was also decreased in the s.c. LLC tumors. On the contrary, disruption of mTORC1 in myeloid cells promoted lung cancer metastasis. Accordingly, immunosuppressive interstitial macrophages/metastasis-associated macrophages (CD11b<sup>+</sup>F4/80<sup>high</sup>) were accumulated in the lungs of Raptor KO mice in the LLC lung metastasis model, leading to decreased Th1 responses. Taken together, our results demonstrate that differential tumor microenvironment dictates the immunological outcomes of myeloid cells, with mTORC1 disruption leading to different tumor growth phenotypes.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">30665937</PMID><DateCompleted><Year>2019</Year><Month>11</Month><Day>12</Day></DateCompleted><DateRevised><Year>2020</Year><Month>03</Month><Day>09</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1550-6606</ISSN><JournalIssue CitedMedium="Internet"><Volume>202</Volume><Issue>5</Issue><PubDate><Year>2019</Year><Month>03</Month><Day>01</Day></PubDate></JournalIssue><Title>Journal of immunology (Baltimore, Md. : 1950)</Title><ISOAbbreviation>J Immunol</ISOAbbreviation></Journal><ArticleTitle>Tumor Microenvironment Modulates Immunological Outcomes of Myeloid Cells with mTORC1 Disruption.</ArticleTitle><Pagination><MedlinePgn>1623-1634</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.4049/jimmunol.1801112</ELocationID><Abstract><AbstractText>The role of the mTOR signaling pathway in different myeloid cell subsets is poorly understood in the context of tumor development. In this study, myeloid cell-specific Raptor knockout (KO) mice were used to determine the roles of mechanistic target of rapamycin complex 1 (mTORC1) in regulating macrophage function from Lewis lung carcinoma (LLC) s.c. tumors and lung tumor metastasis. We found no difference in tumor growth between conditional Raptor KO and control mice in the s.c. tumor models, although depletion of mTORC1 decreased the immunosuppressive function of tumor-associated macrophages (TAM). Despite the decreased immunosuppressive activity of TAM, M1-like TAM differentiation was impaired in the s.c. tumor microenvironment of mTORC1 conditional Raptor KO mice due to downregulated CD115 expression on macrophages. In addition, TNF-α production by mTORC1-deficient myeloid cells was also decreased in the s.c. LLC tumors. On the contrary, disruption of mTORC1 in myeloid cells promoted lung cancer metastasis. Accordingly, immunosuppressive interstitial macrophages/metastasis-associated macrophages (CD11b<sup>+</sup>F4/80<sup>high</sup>) were accumulated in the lungs of Raptor KO mice in the LLC lung metastasis model, leading to decreased Th1 responses. Taken together, our results demonstrate that differential tumor microenvironment dictates the immunological outcomes of myeloid cells, with mTORC1 disruption leading to different tumor growth phenotypes.</AbstractText><CopyrightInformation>Copyright © 2019 by The American Association of Immunologists, Inc.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ding</LastName><ForeName>Chuanlin</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Medicine, James Graham Brown Cancer Center, University of Louisville, Louisville, KY 40202; and Department of Microbiology and Immunology, James Graham Brown Cancer Center, University of Louisville, Louisville, KY 40202 chuanlin.ding@louisville.edu jun.yan@louisville.edu.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sun</LastName><ForeName>Xiaomin</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Medicine, James Graham Brown Cancer Center, University of Louisville, Louisville, KY 40202; and Department of Microbiology and Immunology, James Graham Brown Cancer Center, University of Louisville, Louisville, KY 40202.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wu</LastName><ForeName>Caijun</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Medicine, James Graham Brown Cancer Center, University of Louisville, Louisville, KY 40202; and Department of Microbiology and Immunology, James Graham Brown Cancer Center, University of Louisville, Louisville, KY 40202.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hu</LastName><ForeName>Xiaoling</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Medicine, James Graham Brown Cancer Center, University of Louisville, Louisville, KY 40202; and Department of Microbiology and Immunology, James Graham Brown Cancer Center, University of Louisville, Louisville, KY 40202.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Huang-Ge</ForeName><Initials>HG</Initials><AffiliationInfo><Affiliation>Department of Medicine, James Graham Brown Cancer Center, University of Louisville, Louisville, KY 40202; and Department of Microbiology and Immunology, James Graham Brown Cancer Center, University of Louisville, Louisville, KY 40202.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yan</LastName><ForeName>Jun</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Medicine, James Graham Brown Cancer Center, University of Louisville, Louisville, KY 40202; and Department of Microbiology and Immunology, James Graham Brown Cancer Center, University of Louisville, Louisville, KY 40202 chuanlin.ding@louisville.edu jun.yan@louisville.edu.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>P01 CA163223</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 CA213990</GrantID><Acronym>CA</Acronym><Agency>NCI 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>2019</Year><Month>01</Month><Day>21</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Immunol</MedlineTA><NlmUniqueID>2985117R</NlmUniqueID><ISSNLinking>0022-1767</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber><NameOfSubstance UI="D000076222">Mechanistic Target of Rapamycin Complex 1</NameOfSubstance></Chemical></ChemicalList><CitationSubset>AIM</CitationSubset><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008175" MajorTopicYN="N">Lung Neoplasms</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000076222" MajorTopicYN="N">Mechanistic Target of Rapamycin Complex 1</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018345" MajorTopicYN="N">Mice, Knockout</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008822" MajorTopicYN="N">Mice, 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Huang Ge" uniqKey="Zhang H" first="Huang-Ge" last="Zhang">Huang-Ge Zhang</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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