Tumor Microenvironment Modulates Immunological Outcomes of Myeloid Cells with mTORC1 Disruption.
Identifieur interne : 000367 ( Main/Corpus ); précédent : 000366; suivant : 000368Tumor Microenvironment Modulates Immunological Outcomes of Myeloid Cells with mTORC1 Disruption.
Auteurs : Chuanlin Ding ; Xiaomin Sun ; Caijun Wu ; Xiaoling Hu ; Huang-Ge Zhang ; Jun YanSource :
- Journal of immunology (Baltimore, Md. : 1950) [ 1550-6606 ] ; 2019.
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
Links to Exploration step
pubmed:30665937Le document en format XML
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<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="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Mechanistic Target of Rapamycin Complex 1</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>
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<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>
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<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>
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