Lactic acid in tumor microenvironments causes dysfunction of NKT cells by interfering with mTOR signaling

Cellular metabolism has been shown to regulate differentiation and function of immune cells. Tumor associated immune cells undergo phenotypic and functional alterations due to the change of cellular metabolism in tumor microenvironments. NKT cells are good candidates for immunotherapies against tumo...

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Published in	Science China. Life sciences Vol. 59; no. 12; pp. 1290 - 1296
Main Authors	Xie, Di, Zhu, Shasha, Bai, Li
Format	Journal Article
Language	English
Published	Beijing Science China Press 01.12.2016 Springer Nature B.V
Subjects	Active Transport, Cell Nucleus - drug effects Animals Biomedical and Life Sciences Cell Line, Tumor Cells, Cultured Coculture Techniques Flow Cytometry Humans Hydrogen-Ion Concentration Interferon-gamma - metabolism Interleukin-4 - metabolism Kruppel-Like Transcription Factors - metabolism Lactic Acid - metabolism Lactic Acid - pharmacology Life Sciences Mice, Transgenic Microscopy, Confocal Natural Killer T-Cells - drug effects Natural Killer T-Cells - metabolism Neoplasms - metabolism Neoplasms - pathology Promyelocytic Leukemia Zinc Finger Protein Research Paper Signal Transduction - drug effects TOR Serine-Threonine Kinases - metabolism Tumor Microenvironment lactic acid IFNγ mTOR NKT cell PLZF
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Abstract	Cellular metabolism has been shown to regulate differentiation and function of immune cells. Tumor associated immune cells undergo phenotypic and functional alterations due to the change of cellular metabolism in tumor microenvironments. NKT cells are good candidates for immunotherapies against tumors and have been used in several clinical trials. However, the influences of tumor microenvironments on NKT cell functions remain unclear. In our studies, lactic acid in tumor microenvironments inhibited IFN？ and IL4 productions from NKT cells, and more profound influence on IFN？ was observed. By adjusting the pH of culture medium we fiu-ther showed that, dysfunction of NKT cells could simply be induced by low extracellular pH. Moreover, low extracellular pH inhibited NKT cell functions by inhibiting mammalian target of rapamycin （roTOR） signaling and nuclear translocation of promyelocytic leukemia zinc-finger （PLZF）. Together, our results suggest that tumor acidic microenvironments could interfere with NKT cell functions through metabolic controls.
AbstractList	Cellular metabolism has been shown to regulate differentiation and function of immune cells. Tumor associated immune cells undergo phenotypic and functional alterations due to the change of cellular metabolism in tumor microenvironments. NKT cells are good candidates for immunotherapies against tumors and have been used in several clinical trials. However, the influences of tumor microenvironments on NKT cell functions remain unclear. In our studies, lactic acid in tumor microenvironments inhibited IFNγ and IL4 productions from NKT cells, and more profound influence on IFNγ was observed. By adjusting the pH of culture medium we further showed that, dysfunction of NKT cells could simply be induced by low extracellular pH. Moreover, low extracellular pH inhibited NKT cell functions by inhibiting mammalian target of rapamycin (mTOR) signaling and nuclear translocation of promyelocytic leukemia zinc-finger (PLZF). Together, our results suggest that tumor acidic microenvironments could interfere with NKT cell functions through metabolic controls. Cellular metabolism has been shown to regulate differentiation and function of immune cells. Tumor associated immune cells undergo phenotypic and functional alterations due to the change of cellular metabolism in tumor microenvironments. NKT cells are good candidates for immunotherapies against tumors and have been used in several clinical trials. However, the influences of tumor microenvironments on NKT cell functions remain unclear. In our studies, lactic acid in tumor microenvironments inhibited IFN gamma and IL4 productions from NKT cells, and more profound influence on IFN gamma was observed. By adjusting the pH of culture medium we further showed that, dysfunction of NKT cells could simply be induced by low extracellular pH. Moreover, low extracellular pH inhibited NKT cell functions by inhibiting mammalian target of rapamycin (mTOR) signaling and nuclear translocation of promyelocytic leukemia zinc-finger (PLZF). Together, our results suggest that tumor acidic microenvironments could interfere with NKT cell functions through metabolic controls. Cellular metabolism has been shown to regulate differentiation and function of immune cells. Tumor associated immune cells undergo phenotypic and functional alterations due to the change of cellular metabolism in tumor microenvironments. NKT cells are good candidates for immunotherapies against tumors and have been used in several clinical trials. However, the influences of tumor microenvironments on NKT cell functions remain unclear. In our studies, lactic acid in tumor microenvironments inhibited IFN？ and IL4 productions from NKT cells, and more profound influence on IFN？ was observed. By adjusting the pH of culture medium we fiu-ther showed that, dysfunction of NKT cells could simply be induced by low extracellular pH. Moreover, low extracellular pH inhibited NKT cell functions by inhibiting mammalian target of rapamycin （roTOR） signaling and nuclear translocation of promyelocytic leukemia zinc-finger （PLZF）. Together, our results suggest that tumor acidic microenvironments could interfere with NKT cell functions through metabolic controls.
Author	Di Xie Shasha Zhu Li Bai
AuthorAffiliation	CAS Key Laboratory of lnnate lmmunity and Chronic Disease, CAS Center for Excellence in Molecular Cell Science, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei 230027, China Innovation Center for Cell Signaling Network, Hefei National Laboratory for Physical Sciences at Microscale, Hefei 230027, China
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Notes	11-5841/Q Cellular metabolism has been shown to regulate differentiation and function of immune cells. Tumor associated immune cells undergo phenotypic and functional alterations due to the change of cellular metabolism in tumor microenvironments. NKT cells are good candidates for immunotherapies against tumors and have been used in several clinical trials. However, the influences of tumor microenvironments on NKT cell functions remain unclear. In our studies, lactic acid in tumor microenvironments inhibited IFN？ and IL4 productions from NKT cells, and more profound influence on IFN？ was observed. By adjusting the pH of culture medium we fiu-ther showed that, dysfunction of NKT cells could simply be induced by low extracellular pH. Moreover, low extracellular pH inhibited NKT cell functions by inhibiting mammalian target of rapamycin （roTOR） signaling and nuclear translocation of promyelocytic leukemia zinc-finger （PLZF）. Together, our results suggest that tumor acidic microenvironments could interfere with NKT cell functions through metabolic controls. lactic acid, NKT cell, IFNT, mTOR, PLZF ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
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Snippet	Cellular metabolism has been shown to regulate differentiation and function of immune cells. Tumor associated immune cells undergo phenotypic and functional...
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SubjectTerms	Active Transport, Cell Nucleus - drug effects Animals Biomedical and Life Sciences Cell Line, Tumor Cells, Cultured Coculture Techniques Flow Cytometry Humans Hydrogen-Ion Concentration Interferon-gamma - metabolism Interleukin-4 - metabolism Kruppel-Like Transcription Factors - metabolism Lactic Acid - metabolism Lactic Acid - pharmacology Life Sciences Mice, Transgenic Microscopy, Confocal Natural Killer T-Cells - drug effects Natural Killer T-Cells - metabolism Neoplasms - metabolism Neoplasms - pathology Promyelocytic Leukemia Zinc Finger Protein Research Paper Signal Transduction - drug effects TOR Serine-Threonine Kinases - metabolism Tumor Microenvironment
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Title	Lactic acid in tumor microenvironments causes dysfunction of NKT cells by interfering with mTOR signaling
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