13C tracer analysis reveals the landscape of metabolic checkpoints in human CD8+ T cell differentiation and exhaustion

Naïve T cells remain in an actively maintained state of quiescence until activation by antigenic signals, upon which they start to proliferate and generate effector cells to initiate a functional immune response. Metabolic reprogramming is essential to meet the biosynthetic demands of the differenti...

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Vydáno v:Frontiers in immunology Ročník 14; s. 1267816
Hlavní autoři: Kirchmair, Alexander, Nemati, Niloofar, Lamberti, Giorgia, Trefny, Marcel, Krogsdam, Anne, Siller, Anita, Hörtnagl, Paul, Schumacher, Petra, Sopper, Sieghart, Sandbichler, Adolf, Zippelius, Alfred, Ghesquière, Bart, Trajanoski, Zlatko
Médium: Journal Article
Jazyk:angličtina
Vydáno: Frontiers Media S.A 19.10.2023
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ISSN:1664-3224, 1664-3224
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Abstract Naïve T cells remain in an actively maintained state of quiescence until activation by antigenic signals, upon which they start to proliferate and generate effector cells to initiate a functional immune response. Metabolic reprogramming is essential to meet the biosynthetic demands of the differentiation process, and failure to do so can promote the development of hypofunctional exhausted T cells.IntroductionNaïve T cells remain in an actively maintained state of quiescence until activation by antigenic signals, upon which they start to proliferate and generate effector cells to initiate a functional immune response. Metabolic reprogramming is essential to meet the biosynthetic demands of the differentiation process, and failure to do so can promote the development of hypofunctional exhausted T cells.Here we used 13C metabolomics and transcriptomics to study the metabolism of CD8+ T cells in their complete course of differentiation from naïve over stem-like memory to effector cells and in exhaustion-inducing conditions.MethodsHere we used 13C metabolomics and transcriptomics to study the metabolism of CD8+ T cells in their complete course of differentiation from naïve over stem-like memory to effector cells and in exhaustion-inducing conditions.The quiescence of naïve T cells was evident in a profound suppression of glucose oxidation and a decreased expression of ENO1, downstream of which no glycolytic flux was detectable. Moreover, TCA cycle activity was low in naïve T cells and associated with a downregulation of SDH subunits. Upon stimulation and exit from quiescence, the initiation of cell growth and proliferation was accompanied by differential expression of metabolic enzymes and metabolic reprogramming towards aerobic glycolysis with high rates of nutrient uptake, respiration and lactate production. High flux in anabolic pathways imposed a strain on NADH homeostasis, which coincided with engagement of the proline cycle for mitochondrial redox shuttling. With acquisition of effector functions, cells increasingly relied on glycolysis as opposed to oxidative phosphorylation, which was, however, not linked to changes in mitochondrial abundance. In exhaustion, decreased effector function concurred with a reduction in mitochondrial metabolism, glycolysis and amino acid import, and an upregulation of quiescence-associated genes, TXNIP and KLF2, and the T cell suppressive metabolites succinate and itaconate.ResultsThe quiescence of naïve T cells was evident in a profound suppression of glucose oxidation and a decreased expression of ENO1, downstream of which no glycolytic flux was detectable. Moreover, TCA cycle activity was low in naïve T cells and associated with a downregulation of SDH subunits. Upon stimulation and exit from quiescence, the initiation of cell growth and proliferation was accompanied by differential expression of metabolic enzymes and metabolic reprogramming towards aerobic glycolysis with high rates of nutrient uptake, respiration and lactate production. High flux in anabolic pathways imposed a strain on NADH homeostasis, which coincided with engagement of the proline cycle for mitochondrial redox shuttling. With acquisition of effector functions, cells increasingly relied on glycolysis as opposed to oxidative phosphorylation, which was, however, not linked to changes in mitochondrial abundance. In exhaustion, decreased effector function concurred with a reduction in mitochondrial metabolism, glycolysis and amino acid import, and an upregulation of quiescence-associated genes, TXNIP and KLF2, and the T cell suppressive metabolites succinate and itaconate.Overall, these results identify multiple metabolic features that regulate quiescence, proliferation and effector function, but also exhaustion of CD8+ T cells during differentiation. Thus, targeting these metabolic checkpoints may be a promising therapeutic strategy for both prevention of exhaustion and promotion of stemness of anti-tumor T cells.DiscussionOverall, these results identify multiple metabolic features that regulate quiescence, proliferation and effector function, but also exhaustion of CD8+ T cells during differentiation. Thus, targeting these metabolic checkpoints may be a promising therapeutic strategy for both prevention of exhaustion and promotion of stemness of anti-tumor T cells.
AbstractList IntroductionNaïve T cells remain in an actively maintained state of quiescence until activation by antigenic signals, upon which they start to proliferate and generate effector cells to initiate a functional immune response. Metabolic reprogramming is essential to meet the biosynthetic demands of the differentiation process, and failure to do so can promote the development of hypofunctional exhausted T cells.MethodsHere we used 13C metabolomics and transcriptomics to study the metabolism of CD8+ T cells in their complete course of differentiation from naïve over stem-like memory to effector cells and in exhaustion-inducing conditions. ResultsThe quiescence of naïve T cells was evident in a profound suppression of glucose oxidation and a decreased expression of ENO1, downstream of which no glycolytic flux was detectable. Moreover, TCA cycle activity was low in naïve T cells and associated with a downregulation of SDH subunits. Upon stimulation and exit from quiescence, the initiation of cell growth and proliferation was accompanied by differential expression of metabolic enzymes and metabolic reprogramming towards aerobic glycolysis with high rates of nutrient uptake, respiration and lactate production. High flux in anabolic pathways imposed a strain on NADH homeostasis, which coincided with engagement of the proline cycle for mitochondrial redox shuttling. With acquisition of effector functions, cells increasingly relied on glycolysis as opposed to oxidative phosphorylation, which was, however, not linked to changes in mitochondrial abundance. In exhaustion, decreased effector function concurred with a reduction in mitochondrial metabolism, glycolysis and amino acid import, and an upregulation of quiescence-associated genes, TXNIP and KLF2, and the T cell suppressive metabolites succinate and itaconate. DiscussionOverall, these results identify multiple metabolic features that regulate quiescence, proliferation and effector function, but also exhaustion of CD8+ T cells during differentiation. Thus, targeting these metabolic checkpoints may be a promising therapeutic strategy for both prevention of exhaustion and promotion of stemness of anti-tumor T cells.
Naïve T cells remain in an actively maintained state of quiescence until activation by antigenic signals, upon which they start to proliferate and generate effector cells to initiate a functional immune response. Metabolic reprogramming is essential to meet the biosynthetic demands of the differentiation process, and failure to do so can promote the development of hypofunctional exhausted T cells.IntroductionNaïve T cells remain in an actively maintained state of quiescence until activation by antigenic signals, upon which they start to proliferate and generate effector cells to initiate a functional immune response. Metabolic reprogramming is essential to meet the biosynthetic demands of the differentiation process, and failure to do so can promote the development of hypofunctional exhausted T cells.Here we used 13C metabolomics and transcriptomics to study the metabolism of CD8+ T cells in their complete course of differentiation from naïve over stem-like memory to effector cells and in exhaustion-inducing conditions.MethodsHere we used 13C metabolomics and transcriptomics to study the metabolism of CD8+ T cells in their complete course of differentiation from naïve over stem-like memory to effector cells and in exhaustion-inducing conditions.The quiescence of naïve T cells was evident in a profound suppression of glucose oxidation and a decreased expression of ENO1, downstream of which no glycolytic flux was detectable. Moreover, TCA cycle activity was low in naïve T cells and associated with a downregulation of SDH subunits. Upon stimulation and exit from quiescence, the initiation of cell growth and proliferation was accompanied by differential expression of metabolic enzymes and metabolic reprogramming towards aerobic glycolysis with high rates of nutrient uptake, respiration and lactate production. High flux in anabolic pathways imposed a strain on NADH homeostasis, which coincided with engagement of the proline cycle for mitochondrial redox shuttling. With acquisition of effector functions, cells increasingly relied on glycolysis as opposed to oxidative phosphorylation, which was, however, not linked to changes in mitochondrial abundance. In exhaustion, decreased effector function concurred with a reduction in mitochondrial metabolism, glycolysis and amino acid import, and an upregulation of quiescence-associated genes, TXNIP and KLF2, and the T cell suppressive metabolites succinate and itaconate.ResultsThe quiescence of naïve T cells was evident in a profound suppression of glucose oxidation and a decreased expression of ENO1, downstream of which no glycolytic flux was detectable. Moreover, TCA cycle activity was low in naïve T cells and associated with a downregulation of SDH subunits. Upon stimulation and exit from quiescence, the initiation of cell growth and proliferation was accompanied by differential expression of metabolic enzymes and metabolic reprogramming towards aerobic glycolysis with high rates of nutrient uptake, respiration and lactate production. High flux in anabolic pathways imposed a strain on NADH homeostasis, which coincided with engagement of the proline cycle for mitochondrial redox shuttling. With acquisition of effector functions, cells increasingly relied on glycolysis as opposed to oxidative phosphorylation, which was, however, not linked to changes in mitochondrial abundance. In exhaustion, decreased effector function concurred with a reduction in mitochondrial metabolism, glycolysis and amino acid import, and an upregulation of quiescence-associated genes, TXNIP and KLF2, and the T cell suppressive metabolites succinate and itaconate.Overall, these results identify multiple metabolic features that regulate quiescence, proliferation and effector function, but also exhaustion of CD8+ T cells during differentiation. Thus, targeting these metabolic checkpoints may be a promising therapeutic strategy for both prevention of exhaustion and promotion of stemness of anti-tumor T cells.DiscussionOverall, these results identify multiple metabolic features that regulate quiescence, proliferation and effector function, but also exhaustion of CD8+ T cells during differentiation. Thus, targeting these metabolic checkpoints may be a promising therapeutic strategy for both prevention of exhaustion and promotion of stemness of anti-tumor T cells.
Author Ghesquière, Bart
Zippelius, Alfred
Trefny, Marcel
Nemati, Niloofar
Lamberti, Giorgia
Schumacher, Petra
Krogsdam, Anne
Sandbichler, Adolf
Kirchmair, Alexander
Sopper, Sieghart
Siller, Anita
Trajanoski, Zlatko
Hörtnagl, Paul
AuthorAffiliation 3 NGS Core Facility, Biocenter, Medical University of Innsbruck , Innsbruck , Austria
6 Institute of Zoology, University of Innsbruck , Innsbruck , Austria
8 Metabolomics Core Facility Leuven, Center for Cancer Biology, VIB , Leuven , Belgium
1 Institute of Bioinformatics, Biocenter, Medical University of Innsbruck , Innsbruck , Austria
4 Central Institute for Blood Transfusion and Immunology, Tirol Kliniken GmbH , Innsbruck , Austria
5 Core Facility FACS Sorting, University Clinic for Internal Medicine V, Medical University of Innsbruck , Innsbruck , Austria
7 Laboratory of Applied Mass Spectrometry, Department of Cellular and Molecular Medicine, KU Leuven , Leuven , Belgium
2 Department of Biomedicine, Cancer Immunology, University and University Hospital of Basel , Basel , Switzerland
AuthorAffiliation_xml – name: 1 Institute of Bioinformatics, Biocenter, Medical University of Innsbruck , Innsbruck , Austria
– name: 8 Metabolomics Core Facility Leuven, Center for Cancer Biology, VIB , Leuven , Belgium
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– name: 3 NGS Core Facility, Biocenter, Medical University of Innsbruck , Innsbruck , Austria
– name: 7 Laboratory of Applied Mass Spectrometry, Department of Cellular and Molecular Medicine, KU Leuven , Leuven , Belgium
– name: 6 Institute of Zoology, University of Innsbruck , Innsbruck , Austria
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Cites_doi 10.3390/biomedicines10112809
10.1073/pnas.1920413117
10.1093/nar/gkaa1011
10.1002/eji.202048851
10.2147/BTT.S365490
10.1016/j.ebiom.2016.01.019
10.3389/fchem.2021.669308
10.1038/s41590-020-0791-5
10.1158/2159-8290.CD-22-1276
10.14806/ej.17.1.200
10.1038/s41591-018-0290-5
10.3389/fimmu.2020.01013
10.1038/s41577-021-00537-8
10.1158/1078-0432.CCR-15-1849
10.1038/s41598-020-80933-7
10.1038/s41586-019-1678-1
10.1007/978-1-4939-9236-2_19
10.1146/annurev-cellbio-092910-154237
10.1016/j.celrep.2022.111987
10.1038/s41586-019-1836-5
10.7554/eLife.10769
10.1177/1947601910389604
10.1038/s41598-018-36293-4
10.1038/44385
10.1016/j.immuni.2019.09.003
10.1038/s41590-019-0312-6
10.1016/j.immuni.2020.09.005
10.1016/j.cell.2013.05.016
10.1038/nm.1982
10.1111/j.1537-2995.2007.01233.x
10.1016/j.cmet.2016.06.004
10.1016/j.cmet.2022.06.008
10.1016/j.immuni.2022.02.004
10.1038/s41467-020-17756-7
10.1093/bioinformatics/bts635
10.1038/s41577-020-00478-8
10.1016/j.crimmu.2021.12.002
10.1038/s42255-022-00676-9
10.1371/journal.pone.0104104
10.1126/science.aau0135
10.1093/nar/gkx193
10.1186/s13059-014-0550-8
10.1126/science.abe9977
10.1038/s41598-019-53234-x
10.1016/j.celrep.2022.111639
10.1038/nature25144
10.1016/j.celrep.2022.111138
10.1038/s41577-020-00454-2
10.1038/s42255-022-00730-6
10.1016/j.immuni.2021.02.018
10.1126/science.aay0524
10.4049/jimmunol.1000173
10.1016/j.immuni.2022.12.002
10.1038/s41591-023-02371-y
10.1111/imcb.12517
10.1172/JCI148546
10.26508/lsa.202101081
10.1016/j.celrep.2016.11.065
10.1038/s41589-019-0323-5
10.1038/s41590-022-01171-9
10.1016/j.cell.2015.08.012
10.1073/pnas.0709747104
10.1038/nm1326
10.1038/nm.2446
10.1089/omi.2011.0118
10.4049/jimmunol.1101530
10.1038/s42255-022-00710-w
10.1038/s41467-022-32521-8
10.1038/s41588-019-0557-x
10.1126/sciimmunol.aap9520
10.1126/scisignal.aaz1482
10.1016/j.cmet.2022.02.009
10.1038/s41590-020-0733-2
10.1038/s41467-018-04274-w
10.1038/s41586-021-04248-x
10.1038/s41556-020-00615-4
10.1084/jem.192.7.1027
10.1158/2326-6066.CIR-17-0605
10.1038/s41586-019-1674-5
10.1186/1471-2105-14-7
10.1073/pnas.2023752118
10.1038/s41467-022-35583-w
10.1038/nature10491
10.1016/j.celrep.2022.111193
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Copyright Copyright © 2023 Kirchmair, Nemati, Lamberti, Trefny, Krogsdam, Siller, Hörtnagl, Schumacher, Sopper, Sandbichler, Zippelius, Ghesquière and Trajanoski.
Copyright © 2023 Kirchmair, Nemati, Lamberti, Trefny, Krogsdam, Siller, Hörtnagl, Schumacher, Sopper, Sandbichler, Zippelius, Ghesquière and Trajanoski 2023 Kirchmair, Nemati, Lamberti, Trefny, Krogsdam, Siller, Hörtnagl, Schumacher, Sopper, Sandbichler, Zippelius, Ghesquière and Trajanoski
Copyright_xml – notice: Copyright © 2023 Kirchmair, Nemati, Lamberti, Trefny, Krogsdam, Siller, Hörtnagl, Schumacher, Sopper, Sandbichler, Zippelius, Ghesquière and Trajanoski.
– notice: Copyright © 2023 Kirchmair, Nemati, Lamberti, Trefny, Krogsdam, Siller, Hörtnagl, Schumacher, Sopper, Sandbichler, Zippelius, Ghesquière and Trajanoski 2023 Kirchmair, Nemati, Lamberti, Trefny, Krogsdam, Siller, Hörtnagl, Schumacher, Sopper, Sandbichler, Zippelius, Ghesquière and Trajanoski
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Edited by: Xiong Li, Huazhong University of Science and Technology, China
Reviewed by: Adam Klocperk, Charles University, Czechia; Guang Sheng Ling, The University of Hong Kong, Hong Kong SAR, China
Present address: Marcel Trefny, Division of Clinical Pharmacology, Ludwig-Maximilians-Universität München, Munich, Germany
These authors share first authorship
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References Liu (B14) 2020; 21
Adams (B70) 2016; 17
Wu (B21) 2021; 23
Jansen (B47) 2019; 576
Trefny (B35) 2023; 14
Zhang (B2) 2005; 11
Yuan (B52) 2020; 52
Fuertes Marraco (B10) 2022; 3
Néron (B34) 2007; 47
Jung (B6) 2022; 40
Chang (B63) 2013; 153
Lisci (B71) 2021; 374
Heinrich (B38) 2018; 8
Scholz (B83) 2016; 4
Rath (B43) 2021; 49
Feng (B69) 2022; 13
Cheng (B66) 2023; 5
Elia (B23) 2022; 34
Zarour (B25) 2016; 22
Dobin (B40) 2013; 29
Gupta (B16) 2020; 11
Levring (B77) 2019; 9
ElTanbouly (B13) 2020; 367
Zhao (B81) 2022; 4
Hermans (B30) 2020; 117
Gattinoni (B3) 2011; 17
Fernández-García (B33) 2022; 41
Zhang (B67) 2019; 574
Chapman (B56) 2018; 6
Lunt (B17) 2011; 27
Xu (B60) 2023; 42
Galletti (B48) 2020; 21
Yu (B45) 2012; 16
Corrado (B18) 2022; 132
Agrawal (B37) 2019
Schulz (B19) 2022; 100
Ma (B31) 2019; 51
Gemta (B57) 2019; 4
Nastasi (B58) 2021; 11
Gearty (B7) 2022; 602
Sallusto (B1) 1999; 401
O’Sullivan (B72) 2021; 118
Dickinson (B28) 2023; 13
Rahman (B73) 2021; 4
Miller (B27) 2019; 20
Hänzelmann (B51) 2013; 14
Reznik (B53) 2016; 5
DeBerardinis (B59) 2007; 104
Bresser (B9) 2022; 23
Reina-Campos (B62) 2021; 21
Giles (B49) 2022; 55
Gudgeon (B79) 2022; 40
Levine (B32) 2021; 54
Lee (B41) 2017; 45
Cao (B55) 2014; 9
Lin (B24) 2021; 9
Wu (B64) 2020; 11
ElTanbouly (B12) 2021; 21
Prokhnevska (B4) 2023; 56
Chan (B26) 2022; 10
Freeman (B15) 2000; 192
Schmid (B36) 2010; 184
Pais Ferreira (B5) 2020; 53
Qin (B82) 2019; 15
Muri (B78) 2021; 21
Dabi (B29) 2022; 16
Love (B42) 2014; 15
Ye (B61) 2022; 34
Ho (B20) 2015; 162
Elgort (B75) 2010; 1
Gattinoni (B8) 2009; 15
Vodnala (B84) 2019; 363
Muri (B74) 2018; 9
Johnston (B65) 2019; 574
Muri (B76) 2021; 51
Youngblood (B11) 2017; 552
Martin (B39) 2011; 17
Lampropoulou (B80) 2016; 24
Chu (B50) 2023; 29
Yang (B68) 2023; 5
Hart (B54) 2012; 188
Feucht (B46) 2019; 25
Robinson (B44) 2020; 13
Opitz (B22) 2011; 478
References_xml – volume: 10
  start-page: 2809
  year: 2022
  ident: B26
  article-title: Immune checkpoint molecules and glucose metabolism in HIV-induced T cell exhaustion
  publication-title: Biomedicines
  doi: 10.3390/biomedicines10112809
– volume: 117
  year: 2020
  ident: B30
  article-title: Lactate dehydrogenase inhibition synergizes with IL-21 to promote CD8 + T cell stemness and antitumor immunity
  publication-title: Proc Natl Acad Sci
  doi: 10.1073/pnas.1920413117
– volume: 49
  year: 2021
  ident: B43
  article-title: MitoCarta3.0: an updated mitochondrial proteome now with sub-organelle localization and pathway annotations
  publication-title: Nucleic Acids Res
  doi: 10.1093/nar/gkaa1011
– volume: 51
  year: 2021
  ident: B76
  article-title: The thioredoxin-1 inhibitor Txnip restrains effector T-cell and germinal center B-cell expansion
  publication-title: Eur J Immunol
  doi: 10.1002/eji.202048851
– volume: 16
  start-page: 35
  year: 2022
  ident: B29
  article-title: Targeting metabolic reprogramming of T-cells for enhanced anti-tumor response
  publication-title: Biol Targets Ther
  doi: 10.2147/BTT.S365490
– volume: 4
  start-page: 50
  year: 2016
  ident: B83
  article-title: Modulation of mTOR signalling triggers the formation of stem cell-like memory T cells
  publication-title: EBioMedicine.
  doi: 10.1016/j.ebiom.2016.01.019
– volume: 9
  year: 2021
  ident: B24
  article-title: The emerging application of itaconate: promising molecular targets and therapeutic opportunities
  publication-title: Front Chem
  doi: 10.3389/fchem.2021.669308
– volume: 21
  year: 2020
  ident: B48
  article-title: Two subsets of stem-like CD8+ memory T cell progenitors with distinct fate commitments in humans
  publication-title: Nat Immunol
  doi: 10.1038/s41590-020-0791-5
– volume: 13
  start-page: CD
  year: 2023
  ident: B28
  article-title: A novel autologous CAR-T therapy, YTB323, with preserved T-cell stemness shows enhanced CAR T-cell efficacy in preclinical and early clinical development
  publication-title: Cancer Discovery
  doi: 10.1158/2159-8290.CD-22-1276
– volume: 17
  start-page: 10
  year: 2011
  ident: B39
  article-title: Cutadapt removes adapter sequences from high-throughput sequencing reads
  publication-title: EMBnet.journal.
  doi: 10.14806/ej.17.1.200
– volume: 25
  year: 2019
  ident: B46
  article-title: Calibration of CAR activation potential directs alternative T cell fates and therapeutic potency
  publication-title: Nat Med
  doi: 10.1038/s41591-018-0290-5
– volume: 11
  year: 2020
  ident: B16
  article-title: Metabolic reprogramming in CD8+ T cells during acute viral infections
  publication-title: Front Immunol
  doi: 10.3389/fimmu.2020.01013
– volume: 21
  year: 2021
  ident: B62
  article-title: CD8+ T cell metabolism in infection and cancer
  publication-title: Nat Rev Immunol
  doi: 10.1038/s41577-021-00537-8
– volume: 22
  year: 2016
  ident: B25
  article-title: Reversing T-cell dysfunction and exhaustion in cancer
  publication-title: Clin Cancer Res Off J Am Assoc Cancer Res
  doi: 10.1158/1078-0432.CCR-15-1849
– volume: 11
  start-page: 1458
  year: 2021
  ident: B58
  article-title: Inhibition of succinate dehydrogenase activity impairs human T cell activation and function
  publication-title: Sci Rep
  doi: 10.1038/s41598-020-80933-7
– volume: 574
  year: 2019
  ident: B67
  article-title: Metabolic regulation of gene expression by histone lactylation
  publication-title: Nature
  doi: 10.1038/s41586-019-1678-1
– volume-title: High-Throughput Metabolomics
  year: 2019
  ident: B37
  article-title: El-MAVEN: A Fast, Robust, and User-Friendly Mass Spectrometry Data Processing Engine for Metabolomics
  doi: 10.1007/978-1-4939-9236-2_19
– volume: 27
  year: 2011
  ident: B17
  article-title: Aerobic glycolysis: meeting the metabolic requirements of cell proliferation
  publication-title: Annu Rev Cell Dev Biol
  doi: 10.1146/annurev-cellbio-092910-154237
– volume: 42
  start-page: 111987
  year: 2023
  ident: B60
  article-title: GOT1 regulates CD8+ effector and memory T cell generation
  publication-title: Cell Rep
  doi: 10.1016/j.celrep.2022.111987
– volume: 576
  year: 2019
  ident: B47
  article-title: An intra-tumoral niche maintains and differentiates stem-like CD8 T cells
  publication-title: Nature
  doi: 10.1038/s41586-019-1836-5
– volume: 5
  year: 2016
  ident: B53
  article-title: Mitochondrial DNA copy number variation across human cancers
  publication-title: eLife
  doi: 10.7554/eLife.10769
– volume: 1
  start-page: 893
  year: 2010
  ident: B75
  article-title: Transcriptional and translational downregulation of thioredoxin interacting protein is required for metabolic reprogramming during G1
  publication-title: Genes Cancer
  doi: 10.1177/1947601910389604
– volume: 8
  start-page: 17910
  year: 2018
  ident: B38
  article-title: Correcting for natural isotope abundance and tracer impurity in MS-, MS/MS- and high-resolution-multiple-tracer-data from stable isotope labeling experiments with IsoCorrectoR
  publication-title: Sci Rep
  doi: 10.1038/s41598-018-36293-4
– volume: 401
  year: 1999
  ident: B1
  article-title: Two subsets of memory T lymphocytes with distinct homing potentials and effector functions
  publication-title: Nature
  doi: 10.1038/44385
– volume: 51
  start-page: 856
  year: 2019
  ident: B31
  article-title: Metabolic profiling using stable isotope tracing reveals distinct patterns of glucose utilization by physiologically activated CD8+ T cells
  publication-title: Immunity
  doi: 10.1016/j.immuni.2019.09.003
– volume: 20
  year: 2019
  ident: B27
  article-title: Subsets of exhausted CD8+ T cells differentially mediate tumor control and respond to checkpoint blockade
  publication-title: Nat Immunol
  doi: 10.1038/s41590-019-0312-6
– volume: 53
  start-page: 985
  year: 2020
  ident: B5
  article-title: Central memory CD8+ T cells derive from stem-like Tcf7hi effector cells in the absence of cytotoxic differentiation
  publication-title: Immunity
  doi: 10.1016/j.immuni.2020.09.005
– volume: 153
  year: 2013
  ident: B63
  article-title: Posttranscriptional control of T cell effector function by aerobic glycolysis
  publication-title: Cell
  doi: 10.1016/j.cell.2013.05.016
– volume: 15
  year: 2009
  ident: B8
  article-title: Wnt signaling arrests effector T cell differentiation and generates CD8+ memory stem cells
  publication-title: Nat Med
  doi: 10.1038/nm.1982
– volume: 47
  year: 2007
  ident: B34
  article-title: Characterization of mononuclear cells remaining in the leukoreduction system chambers of apheresis instruments after routine platelet collection: a new source of viable human blood cells
  publication-title: Transfusion (Paris)
  doi: 10.1111/j.1537-2995.2007.01233.x
– volume: 24
  year: 2016
  ident: B80
  article-title: Itaconate links inhibition of succinate dehydrogenase with macrophage metabolic remodeling and regulation of inflammation
  publication-title: Cell Metab
  doi: 10.1016/j.cmet.2016.06.004
– volume: 34
  start-page: 1137
  year: 2022
  ident: B23
  article-title: Tumor cells dictate anti-tumor immune responses by altering pyruvate utilization and succinate signaling in CD8+ T cells
  publication-title: Cell Metab
  doi: 10.1016/j.cmet.2022.06.008
– volume: 55
  start-page: 557
  year: 2022
  ident: B49
  article-title: Human epigenetic and transcriptional T cell differentiation atlas for identifying functional T cell-specific enhancers
  publication-title: Immunity
  doi: 10.1016/j.immuni.2022.02.004
– volume: 11
  start-page: 4113
  year: 2020
  ident: B64
  article-title: T-cells produce acidic niches in lymph nodes to suppress their own effector functions
  publication-title: Nat Commun
  doi: 10.1038/s41467-020-17756-7
– volume: 29
  start-page: 15
  year: 2013
  ident: B40
  article-title: STAR: ultrafast universal RNA-seq aligner
  publication-title: Bioinforma Oxf Engl
  doi: 10.1093/bioinformatics/bts635
– volume: 21
  year: 2021
  ident: B78
  article-title: Redox regulation of immunometabolism
  publication-title: Nat Rev Immunol
  doi: 10.1038/s41577-020-00478-8
– volume: 3
  start-page: 1
  year: 2022
  ident: B10
  article-title: Shared acute phase traits in effector and memory human CD8 T cells
  publication-title: Curr Res Immunol
  doi: 10.1016/j.crimmu.2021.12.002
– volume: 4
  year: 2022
  ident: B81
  article-title: Myeloid-derived itaconate suppresses cytotoxic CD8+ T cells and promotes tumour growth
  publication-title: Nat Metab
  doi: 10.1038/s42255-022-00676-9
– volume: 9
  year: 2014
  ident: B55
  article-title: Metabolic Reprogramming towards Aerobic Glycolysis Correlates with Greater Proliferative Ability and Resistance to Metabolic Inhibition in CD8 versus CD4 T Cells
  publication-title: PLoS One
  doi: 10.1371/journal.pone.0104104
– volume: 363
  year: 2019
  ident: B84
  article-title: T cell stemness and dysfunction in tumors are triggered by a common mechanism
  publication-title: Science
  doi: 10.1126/science.aau0135
– volume: 45
  year: 2017
  ident: B41
  article-title: NGSCheckMate: software for validating sample identity in next-generation sequencing studies within and across data types
  publication-title: Nucleic Acids Res
  doi: 10.1093/nar/gkx193
– volume: 15
  start-page: 550
  year: 2014
  ident: B42
  article-title: Moderated estimation of fold change and dispersion for RNA-seq data with DESeq2
  publication-title: Genome Biol
  doi: 10.1186/s13059-014-0550-8
– volume: 374
  year: 2021
  ident: B71
  article-title: Mitochondrial translation is required for sustained killing by cytotoxic T cells
  publication-title: Science
  doi: 10.1126/science.abe9977
– volume: 9
  start-page: 16725
  year: 2019
  ident: B77
  article-title: Tumor necrosis factor induces rapid down-regulation of TXNIP in human T cells
  publication-title: Sci Rep
  doi: 10.1038/s41598-019-53234-x
– volume: 41
  start-page: 111639
  year: 2022
  ident: B33
  article-title: CD8+ T cell metabolic rewiring defined by scRNA-seq identifies a critical role of ASNS expression dynamics in T cell differentiation
  publication-title: Cell Rep
  doi: 10.1016/j.celrep.2022.111639
– volume: 552
  year: 2017
  ident: B11
  article-title: Effector CD8 T cells dedifferentiate into long-lived memory cells
  publication-title: Nature
  doi: 10.1038/nature25144
– volume: 40
  start-page: 111138
  year: 2022
  ident: B6
  article-title: The generation of stem cell-like memory cells early after BNT162b2 vaccination is associated with durability of memory CD8+ T cell responses
  publication-title: Cell Rep
  doi: 10.1016/j.celrep.2022.111138
– volume: 21
  year: 2021
  ident: B12
  article-title: Rethinking peripheral T cell tolerance: checkpoints across a T cell’s journey
  publication-title: Nat Rev Immunol
  doi: 10.1038/s41577-020-00454-2
– volume: 5
  year: 2023
  ident: B66
  article-title: Extracellular acidosis restricts one-carbon metabolism and preserves T cell stemness
  publication-title: Nat Metab
  doi: 10.1038/s42255-022-00730-6
– volume: 54
  start-page: 829
  year: 2021
  ident: B32
  article-title: Single-cell analysis by mass cytometry reveals metabolic states of early-activated CD8+ T cells during the primary immune response
  publication-title: Immunity
  doi: 10.1016/j.immuni.2021.02.018
– volume: 367
  year: 2020
  ident: B13
  article-title: VISTA is a checkpoint regulator for naïve T cell quiescence and peripheral tolerance
  publication-title: Science
  doi: 10.1126/science.aay0524
– volume: 184
  year: 2010
  ident: B36
  article-title: Evidence for a TCR affinity threshold delimiting maximal CD8 T cell function
  publication-title: J Immunol
  doi: 10.4049/jimmunol.1000173
– volume: 56
  start-page: 107
  year: 2023
  ident: B4
  article-title: CD8+ T cell activation in cancer comprises an initial activation phase in lymph nodes followed by effector differentiation within the tumor
  publication-title: Immunity
  doi: 10.1016/j.immuni.2022.12.002
– volume: 29
  year: 2023
  ident: B50
  article-title: Pan-cancer T cell atlas links a cellular stress response state to immunotherapy resistance
  publication-title: Nat Med
  doi: 10.1038/s41591-023-02371-y
– volume: 100
  year: 2022
  ident: B19
  article-title: Mastering an exhausting marathon: how CD8+ T cells fine-tune metabolic fitness
  publication-title: Immunol Cell Biol
  doi: 10.1111/imcb.12517
– volume: 132
  year: 2022
  ident: B18
  article-title: Targeting memory T cell metabolism to improve immunity
  publication-title: J Clin Invest
  doi: 10.1172/JCI148546
– volume: 4
  year: 2021
  ident: B73
  article-title: Elevated glycolysis imparts functional ability to CD8 + T cells in HIV infection
  publication-title: Life Sci Alliance
  doi: 10.26508/lsa.202101081
– volume: 17
  year: 2016
  ident: B70
  article-title: Anabolism-associated mitochondrial stasis driving lymphocyte differentiation over self-renewal
  publication-title: Cell Rep
  doi: 10.1016/j.celrep.2016.11.065
– volume: 15
  year: 2019
  ident: B82
  article-title: S-glycosylation-based cysteine profiling reveals regulation of glycolysis by itaconate
  publication-title: Nat Chem Biol
  doi: 10.1038/s41589-019-0323-5
– volume: 23
  start-page: 791
  year: 2022
  ident: B9
  article-title: Replicative history marks transcriptional and functional disparity in the CD8+ T cell memory pool
  publication-title: Nat Immunol
  doi: 10.1038/s41590-022-01171-9
– volume: 162
  year: 2015
  ident: B20
  article-title: Phosphoenolpyruvate is a metabolic checkpoint of anti-tumor T cell responses
  publication-title: Cell
  doi: 10.1016/j.cell.2015.08.012
– volume: 104
  year: 2007
  ident: B59
  article-title: Beyond aerobic glycolysis: Transformed cells can engage in glutamine metabolism that exceeds the requirement for protein and nucleotide synthesis
  publication-title: Proc Natl Acad Sci
  doi: 10.1073/pnas.0709747104
– volume: 11
  year: 2005
  ident: B2
  article-title: Host-reactive CD8+ memory stem cells in graft-versus-host disease
  publication-title: Nat Med
  doi: 10.1038/nm1326
– volume: 17
  year: 2011
  ident: B3
  article-title: A human memory T cell subset with stem cell–like properties
  publication-title: Nat Med
  doi: 10.1038/nm.2446
– volume: 16
  year: 2012
  ident: B45
  article-title: clusterProfiler: an R package for comparing biological themes among gene clusters
  publication-title: Omics J Integr Biol
  doi: 10.1089/omi.2011.0118
– volume: 188
  year: 2012
  ident: B54
  article-title: Kruppel-like factors in lymphocyte biology
  publication-title: J Immunol Baltim Md 1950
  doi: 10.4049/jimmunol.1101530
– volume: 5
  start-page: 61
  year: 2023
  ident: B68
  article-title: Lactylome analysis suggests lactylation-dependent mechanisms of metabolic adaptation in hepatocellular carcinoma
  publication-title: Nat Metab
  doi: 10.1038/s42255-022-00710-w
– volume: 13
  start-page: 4981
  year: 2022
  ident: B69
  article-title: Lactate increases stemness of CD8 + T cells to augment anti-tumor immunity
  publication-title: Nat Commun
  doi: 10.1038/s41467-022-32521-8
– volume: 52
  year: 2020
  ident: B52
  article-title: Comprehensive molecular characterization of mitochondrial genomes in human cancers
  publication-title: Nat Genet
  doi: 10.1038/s41588-019-0557-x
– volume: 4
  year: 2019
  ident: B57
  article-title: Impaired enolase 1 glycolytic activity restrains effector functions of tumor-infiltrating CD8 + T cells
  publication-title: Sci Immunol
  doi: 10.1126/sciimmunol.aap9520
– volume: 13
  year: 2020
  ident: B44
  article-title: An atlas of human metabolism
  publication-title: Sci Signal
  doi: 10.1126/scisignal.aaz1482
– volume: 34
  start-page: 595
  year: 2022
  ident: B61
  article-title: A genome-scale gain-of-function CRISPR screen in CD8 T cells identifies proline metabolism as a means to enhance CAR-T therapy
  publication-title: Cell Metab
  doi: 10.1016/j.cmet.2022.02.009
– volume: 21
  year: 2020
  ident: B14
  article-title: Neuropilin-1 is a T cell memory checkpoint limiting long-term antitumor immunity
  publication-title: Nat Immunol
  doi: 10.1038/s41590-020-0733-2
– volume: 9
  start-page: 1851
  year: 2018
  ident: B74
  article-title: The thioredoxin-1 system is essential for fueling DNA synthesis during T-cell metabolic reprogramming and proliferation
  publication-title: Nat Commun
  doi: 10.1038/s41467-018-04274-w
– volume: 602
  year: 2022
  ident: B7
  article-title: An autoimmune stem-like CD8 T cell population drives type 1 diabetes
  publication-title: Nature
  doi: 10.1038/s41586-021-04248-x
– volume: 23
  start-page: 75
  year: 2021
  ident: B21
  article-title: Asparagine enhances LCK signalling to potentiate CD8+ T-cell activation and anti-tumour responses
  publication-title: Nat Cell Biol
  doi: 10.1038/s41556-020-00615-4
– volume: 192
  year: 2000
  ident: B15
  article-title: Engagement of the pd-1 immunoinhibitory receptor by a novel B7 family member leads to negative regulation of lymphocyte activation
  publication-title: J Exp Med
  doi: 10.1084/jem.192.7.1027
– volume: 6
  year: 2018
  ident: B56
  article-title: Hallmarks of T-cell exit from quiescence
  publication-title: Cancer Immunol Res
  doi: 10.1158/2326-6066.CIR-17-0605
– volume: 574
  year: 2019
  ident: B65
  article-title: VISTA is an acidic pH-selective ligand for PSGL-1
  publication-title: Nature
  doi: 10.1038/s41586-019-1674-5
– volume: 14
  start-page: 7
  year: 2013
  ident: B51
  article-title: GSVA: gene set variation analysis for microarray and RNA-seq data
  publication-title: BMC Bioinf
  doi: 10.1186/1471-2105-14-7
– volume: 118
  year: 2021
  ident: B72
  article-title: Fever supports CD8 + effector T cell responses by promoting mitochondrial translation
  publication-title: Proc Natl Acad Sci
  doi: 10.1073/pnas.2023752118
– volume: 14
  start-page: 86
  year: 2023
  ident: B35
  article-title: Deletion of SNX9 alleviates CD8 T cell exhaustion for effective cellular cancer immunotherapy
  publication-title: Nat Commun
  doi: 10.1038/s41467-022-35583-w
– volume: 478
  start-page: 197
  year: 2011
  ident: B22
  article-title: An endogenous tumour-promoting ligand of the human aryl hydrocarbon receptor
  publication-title: Nature
  doi: 10.1038/nature10491
– volume: 40
  start-page: 111193
  year: 2022
  ident: B79
  article-title: Succinate uptake by T cells suppresses their effector function via inhibition of mitochondrial glucose oxidation
  publication-title: Cell Rep
  doi: 10.1016/j.celrep.2022.111193
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Snippet Naïve T cells remain in an actively maintained state of quiescence until activation by antigenic signals, upon which they start to proliferate and generate...
IntroductionNaïve T cells remain in an actively maintained state of quiescence until activation by antigenic signals, upon which they start to proliferate and...
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StartPage 1267816
SubjectTerms 13C tracer analysis
differentiation
exhaustion
Immunology
immunometabolism
RNA sequencing
stem cell memory cells
Title 13C tracer analysis reveals the landscape of metabolic checkpoints in human CD8+ T cell differentiation and exhaustion
URI https://www.proquest.com/docview/2886601367
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