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The Transcription Factor Myc Controls Metabolic Reprogramming upon T Lymphocyte Activation
Open accessAbstract
To fulfill the bioenergetic and biosynthetic demand of proliferation, T cells reprogram their metabolic pathways from fatty acid β-oxidation and pyruvate oxidation via the TCA cycle to the glycolytic, pentose-phosphate, and glutaminolytic pathways. Two of the top-ranked candidate transcription factors potentially responsible for the activation-induced T cell metabolic transcriptome, HIF1α and Myc, were induced upon T cell activation, but only the acute deletion of Myc markedly inhibited activation-induced glycolysis and glutaminolysis in T cells. Glutamine deprivation compromised activation-induced T cell growth and proliferation, and this was partially replaced by nucleotides and polyamines, implicating glutamine as an important source for biosynthetic precursors in active T cells. Metabolic tracer analysis revealed a Myc-dependent metabolic pathway linking glutaminolysis to the biosynthesis of polyamines. Therefore, a Myc-dependent global metabolic transcriptome drives metabolic reprogramming in activated, primary T lymphocytes. This may represent a general mechanism for metabolic reprogramming under patho-physiological conditions.
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“Transcription factor enrichment analysis73 revealed that formate-induced transcriptional changes were linked with an enrichment in transcription factors regulating proliferation and metabolism (e.g.: Myc, Max, Myb)74, effector function (e.g.: Fos, Rela, Stat1, Cebpb)75–77 as well as differentiation and epigenetic control (e.g.: Ets1, Yy1, Pou2f2)78 (Figure 6M).”
From Exercise-induced microbiota metabolite enhances CD8 T cell antitumor immunity promoting immunotherapy efficacy (2025) · cites this paper as [74]
In the citing paper
“Glutamine anaplerosis is critical for meeting the energetic requirements of proliferative cells, such as T cells during the transition from quiescent naïve T cells to effector cells, and in cancers, particularly with MYC elevation.32,36,37”
From The multifaceted contributions of mitochondria to cellular metabolism (2018) · cites this paper as [36]
In the citing paper
“In addition, catabolic pathways of ATP generation such as fatty acid β-oxidation are actively suppressed (9).”
From Fueling Immunity: Insights into Metabolism and Lymphocyte Function (2013) · cites this paper as [9]
In the citing paper
“It is important to note that OXPHOS is still engaged in TEFF cells (9); however, the production of lactate from pyruvate by aerobic glycolysis is the dominant pathway of glucose metabolism in TEFF cells.”
From Fueling Immunity: Insights into Metabolism and Lymphocyte Function (2013) · cites this paper as [9]
In the citing paper
“TCR-mediated up-regulation of the transcription factors c-Myc (9) and estrogen-related receptor α (ERRα) (10) enhances the expression of genes involved in intermediary metabolism.”
From Fueling Immunity: Insights into Metabolism and Lymphocyte Function (2013) · cites this paper as [9]
In the citing paper
“T cell activation promotes a rapid increase in glucose flux through the oxidative PPP (9).”
From Fueling Immunity: Insights into Metabolism and Lymphocyte Function (2013) · cites this paper as [9]
In the citing paper
“Glutamine transporters (SNAT1 and SNAT2) as well as key glutaminolysis enzymes (GLS, GPT, GOT, and GLUD) are up-regulated early after T cell activation similar to glycolysis genes (7, 9); several groups have correlated these changes in gene expression to enhanced glutaminolytic flux in lymphocytes (9, 53).”
From Fueling Immunity: Insights into Metabolism and Lymphocyte Function (2013) · cites this paper as [9]
In the citing paper
“Glutamine transporters (SNAT1 and SNAT2) as well as key glutaminolysis enzymes (GLS, GPT, GOT, and GLUD) are up-regulated early after T cell activation similar to glycolysis genes (7, 9); several groups have correlated these changes in gene expression to enhanced glutaminolytic flux in lymphocytes (9, 53).”
From Fueling Immunity: Insights into Metabolism and Lymphocyte Function (2013) · cites this paper as [9]
In the citing paper
“Hif-1α is not required for the initiation of aerobic glycolysis in activated T cells; instead, c-Myc is uniquely required for this metabolic shift [111].”
From Hypoxia and hypoxia-inducible factors as regulators of T cell development, differentiation, and function (2013) · cites this paper as [111]
In the citing paper
“Hif-1α is not required for the initiation of aerobic glycolysis in activated T cells; instead, c-Myc is uniquely required for this metabolic shift [111].”
From Hypoxia and hypoxia-inducible factors as regulators of T cell development, differentiation, and function (2013) · cites this paper as [111]
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Citations
Cites
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BackgroundCD28-inducible transcription factor DEC1 is required for efficient autoreactive CD4+ T cell response
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“In particular, the induction of glycolysis, glutaminolysis, and the lipid biosynthesis pathway are required for effector T cell differentiation (Pearce et al., 2013; Wang et al., 2011).”
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“To meet bioenergetic and biosynthetic demand during T cell growth and proliferation, glutaminolysis replenishes the anapleurotic substrate α-KG that fuels OXPHOS via the TCA cycle and also provides sources of nitrogen and carbon to support the biosynthesis of nonessential amino acids, lipids, nucleotides, and polyamin…”
BackgroundInfluentialSelf-citationCross-Talk Between the Tumor Microenvironment, Extracellular Matrix, and Cell Metabolism in Cancer
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“In parallel, derailed function of the oncogenic protein c-myc induces the expression of glutamine transporters and glutamine-utilizing enzymes (16, 17).”
BackgroundReshaping the tumor immune microenvironment to improve CAR-T cell-based cancer immunotherapy
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“Upon encountering an antigen, the T cell receptor (TCR) and CD28 synergistically activate the PI3K–AKT–mTOR pathway, effectively activating transcription factors (e.g., HIF-1α, c-MYC) to upregulate the expression of glucose transporter type 1 (GLUT1) and promote glycolysis [65].”
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“This was of specific interest because previous studies have shown that oncogenic c-Myc, or N-Myc, induces increased expression of the glutamine transporter SLC1A5, and dependency upon it for survival in Myc-activated cells[26].”
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Cancer-associated adipocytes as immunomodulators in cancer
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“After TCR activation and costimulation, the PI3K-Akt pathway and the key metabolic regulators mTOR and c-myc upregulate the glucose uptake and glycolysis closely in mouse CD8+ T cells [184, 188].”
BackgroundMyoD Regulates Skeletal Muscle Oxidative Metabolism Cooperatively with Alternative NF-κB
Shintaku, J., Peterson, J. M., Talbert, E. E., Gu, J.-M., Ladner, K. J., Williams, D. R., Mousavi, K., Wang, R., Sartorelli, V., & Guttridge, D. C. (2016) · Cell Reports · doi:10.1016/j.celrep.2016.09.010 · Cited by 108
“[9,10-(3)H] palmitic acid (Wang et al., 2011) (illustrated in Figures 2D and 2E).”
Self-citationReductive carboxylation epigenetically instructs T cell differentiation
Jaccard, A., Wyss, T., Maldonado‐Pérez, N., Rath, J. A., Bevilacqua, A., Peng, J.-J., Lepez, A., Gunten, C. V., Franco, F., Kao, K., et al. (2023) · Nature · doi:10.1038/s41586-023-06546-y · Cited by 105
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“Also, activated T cells display increased shunting of carbons into alternative metabolic circuits, such as the pentose phosphate pathway (46).”
BackgroundKumar, V. (2018) · European Journal of Cell Biology · doi:10.1016/j.ejcb.2018.05.001 · Cited by 106
Lupus-associated atypical memory B cells are mTORC1-hyperactivated and functionally dysregulated
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“These are usually short-lived events that rely primarily on glycolysis for their energy demands (58, 59), which is also observed in cytokine-activated lymphocytes (60).”
BackgroundLactate: The Mediator of Metabolism and Immunosuppression
Zhang, Y., Zhai, Z., Duan, J., Wang, X., Zhong, J., Wu, L., Li, A., Cao, M., Wu, Y., Shi, H., et al. (2022) · Frontiers in Endocrinology · doi:10.3389/fendo.2022.901495 · Cited by 108
“It not only inhibits glycolysis by suppressing the oncogene Myc but also regulates LDH to promote the conversion of lactate to pyruvate and even drives lipid oxidation metabolism to promote OXPHOS, which endows Treg with inhibitory activity (32, 78, 79).”
BackgroundSMYD2-Mediated Histone Methylation Contributes to HIV-1 Latency
Boehm, D., Jeng, M. Y., Camus, G., Gramatica, A., Schwarzer, R., Johnson, J. R., Hull, P. A., Montaño, M., Sakane, N., Pagans, S., et al. (2017) · Cell Host & Microbe · doi:10.1016/j.chom.2017.04.011 · Cited by 100
Metabolic waypoints during T cell differentiation
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“T cell activation also causes an increase in glutamine uptake 19 , and this is driven by the transcription factor Myc 20 .”
The tyrosine phosphatase PTPN22 discriminates weak self peptides from strong agonist TCR signals
Salmond, R. J., Brownlie, R. J., Morrison, V. L., & Zamoyska, R. (2014) · Nature Immunology · doi:10.1038/ni.2958 · Cited by 101
Metabolic reprograming of anti-tumor immunity
Sukumar, M., Kishton, R. J., & Restifo, N. P. (2017) · Current Opinion in Immunology · doi:10.1016/j.coi.2017.03.011 · Cited by 103
Yang, R., Li, X., Wu, Y., Zhang, G., Liu, X., Li, Y., Bao, Y., Yang, W., & Cui, H. (2020) · Oncogene · doi:10.1038/s41388-020-1199-2 · Cited by 101
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Very‐low‐carbohydrate diet enhances human T‐cell immunity through immunometabolic reprogramming
Hirschberger, S., Strauß, G., Effinger, D., Marstaller, X., Ferstl, A., Müller, M. B., Wu, T., Hübner, M., Rahmel, T., Mascolo, H., et al. (2021) · EMBO Molecular Medicine · doi:10.15252/emmm.202114323 · Cited by 99
“It is conceivable that KD could also increase glutaminolysis, another ATP-generating pathway used by T cells (Wang et al, 2011; Wang & Green, 2012), for example, by increasing activity of glutamate dehydrogenase via SIRT4 inhibition (Li et al, 2011; Min et al, 2018).”
BackgroundmTOR and lymphocyte metabolism
Zeng, H., & Chi, H. (2013) · Current Opinion in Immunology · doi:10.1016/j.coi.2013.05.002 · Cited by 101
Self-citationT Cells and Cancer: How Metabolism Shapes Immunity
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“Proc Natl Acad Sci U S A (2002) 99(25):16168–73.”
BackgroundRewiring mitochondrial metabolism to counteract exhaustion of CAR-T cells
Huang, Y., Si, X., Shao, M., Teng, X., Xiao, G., & Huang, H. (2022) · Journal of Hematology & Oncology · doi:10.1186/s13045-022-01255-x · Cited by 110
“In addition, the exhausted T cell phenotype has been related to Myc, which drives a transcription program that reduces glucose catabolism and glutamine oxidation after T cell activation [83, 84].”
BackgroundThe obesity-related pathology and Th17 cells
Endo, Y., Yokote, K., & Nakayama, T. (2016) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-016-2399-3 · Cited by 102
“in these pathways in activated T cells [73].”
BackgroundInfluentialMitochondrial dysfunction in ocular disease: Focus on glaucoma
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“Because the proto-oncogene c-Myc, a transcription factor downstream of MAPK/Erk signaling, is a sophisticated regulator of glycolysis in mammals (31, 49, 50), we are tempted to investigated the potential role of MAPK/Erk activity in T-cell metabolism of fish.”
BackgroundHypoxia-inducible factors regulate T cell metabolism and function
Phan, A. T., & Goldrath, A. W. (2015) · Molecular Immunology · doi:10.1016/j.molimm.2015.08.004 · Cited by 103
Metabolic Stress in the Immune Function of T Cells, Macrophages and Dendritic Cells
Domblides, C., Lartigue, L., & Faustin, B. (2018) · Cells · doi:10.3390/cells7070068 · Cited by 99
“Furthermore, c-Myc favors glucose-derived citrate production for its use by fatty-acid synthesis [29].”
BackgroundMethodMitochondrial Dysfunction and the Aging Immune System
McGuire, P. J. (2019) · Biology · doi:10.3390/biology8020026 · Cited by 103
“This is done despite the presence of oxygen, and is termed aerobic glycolysis or Warburg metabolism [50,56,60].”
Ketelhuth, D. F. J., Lutgens, E., Bäck, M., Binder, C. J., den Bossche, J. V., Daniel, C., Dumitriu, I. E., Hoefer, I. E., Libby, P., O'Neill, L. A. J., et al. (2019) · Cardiovascular Research · doi:10.1093/cvr/cvz166 · Cited by 104
CD28 costimulation drives tumor-infiltrating T cell glycolysis to promote inflammation
Beckermann, K. E., Hongo, R. A., Ye, X., Young, K. L., Carbonell, K., Contreras, D. C., Siska, P. J., Barone, S. M., Roe, C. E., Smith, C. C., et al. (2020) · JCI Insight · doi:10.1172/jci.insight.138729 · Cited by 103
“This bioenergetic switch is consistent with known Myc regulation of metabolic reprogramming during T cell activation (6).”
Regulation of Immune Cell Functions by Metabolic Reprogramming
Kim, J. (2018) · Journal of Immunology Research · doi:10.1155/2018/8605471 · Cited by 97
“M2-like activated macrophages exploit fatty acid oxidation (FAO) to fuel OXPHOS rather than aerobic glycolysis for ATP production [30–32].”
InfluentialmTOR and Aging: An Old Fashioned Dress
Stallone, G., Infante, B., Prisciandaro, C., & Grandaliano, G. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20112774 · Cited by 97
“Abbreviations: 4EBP1 (Eukaryotic translation initiation factor) 4E binding protein 1 AKT Proteine kinase B AMBRA1 Activating molecule in Beclin-1 regulated autophagy AMP Adenosinmonophosphate AMPK Adenosinmonophosphate-activated protein kinase ATP Adenosintriphosphate Bcl2 B-cell lymphoma 2 BlyS B lymphocyte Simulator…”
BackgroundInfluentialThe role of the electron transport chain in immunity
Yin, M., & O’Neill, L. A. J. (2021) · The FASEB Journal · doi:10.1096/fj.202101161r · Cited by 102
The Intercellular Metabolic Interplay between Tumor and Immune Cells
Wang, T., Liu, G., & Wang, R. (2014) · Frontiers in Immunology · doi:10.3389/fimmu.2014.00358 · Cited by 96
Self-citationCretenet, G., Clerc, I., Matias, M. I., Loisel‐Meyer, S., Craveiro, M., Oburoglu, L., Kinet, S., Mongellaz, C., Dardalhon, V., & Taylor, N. N. (2016) · Scientific Reports · doi:10.1038/srep24129 · Cited by 97
“Division profiles of cells expressing different levels of Glut1 were assessed on gated subsets, denoted as Glut1- (1), Glut1-Lo (2), Glut1-Med (3) and Glut1-Hi (4), and the number of division peaks are indicated.”
BackgroundMetabolic regulation of immune responses: therapeutic opportunities
Aßmann, N., & Finlay, D. K. (2016) · Journal of Clinical Investigation · doi:10.1172/jci83005 · Cited by 97
mTOR, linking metabolism and immunity
Xu, X., Ye, L., Araki, K., & Ahmed, R. (2012) · Seminars in Immunology · doi:10.1016/j.smim.2012.12.005 · Cited by 99
“Activated T cells switch from catabolic to anabolic in their metabolism, utilizing aerobic glycolysis and glutaminolysis as a major supply of ATP as well as metabolic intermediates for fueling the fast synthesis of proteins, lipids, nucleotides and other biosynthetic products. mTORC1 has been shown to be involved in t…”
BackgroundGM-CSF Induces Inflammatory Macrophages by Regulating Glycolysis and Lipid Metabolism
Na, Y. R., Gu, G., Jung, D., Kim, Y. W., Na, J., Woo, J. S., Cho, J., Youn, H., & Seok, S. H. (2016) · The Journal of Immunology · doi:10.4049/jimmunol.1600745 · Cited by 97
“Tofind amajor transcription factor that plays a role in the phenotype of GM-CSF–primed macrophages, we examined two proteins, HIF1a and c-myc, because they have been investigated for their metabolic effect (26).”
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Regulation of CD8+ T memory and exhaustion by the mTOR signals
Chen, Y., Xu, Z., Sun, H., Ouyang, X., Han, Y., Yu, H., Wu, N., Xie, Y., & Su, B. (2023) · Cellular and Molecular Immunology · doi:10.1038/s41423-023-01064-3 · Cited by 101
“MYC-de fi cient T cells exhibit defects in glucose and glutamine metabolism and cannot proliferate or differentiate [131, 227].”
Backgroundc-Myc-induced transcription factor AP4 is required for host protection mediated by CD8+ T cells
Chou, C., Pinto, A. K., Curtis, J. D., Persaud, S. P., Cella, M., Lin, C., Edelson, B. T., Allen, P. M., Colonna, M., Pearce, E. L., et al. (2014) · Nature Immunology · doi:10.1038/ni.2943 · Cited by 97
Nutrient and Metabolic Sensing in T Cell Responses
Wei, J., Raynor, J. L., Nguyen, T.-L. M., & Chi, H. (2017) · Frontiers in Immunology · doi:10.3389/fimmu.2017.00247 · Cited by 101
“Furthermore, the loss in c-Myc expression in CD8+ T cells correlates with impaired glucose, glutamine, and arginine uptake and impaired glycolytic metabolism, which promote proper CD8+ T cell effector function (38, 42).”
BackgroundSelf-citationCholesterol Metabolism in T Cells
Bietz, A., Zhu, H., Xue, M., & Xu, C. (2017) · Frontiers in Immunology · doi:10.3389/fimmu.2017.01664 · Cited by 99
Ushio‐Fukai, M., Ash, D., Nagarkoti, S., de Chantemèle, E. J. B., Fulton, D. J., & Fukai, T. (2021) · Antioxidants and Redox Signaling · doi:10.1089/ars.2020.8161 · Cited by 99
“Moreover, regulatory T cells (Tregs) activate AMPK and depend on lipid oxidation for their energy requirements (237, 257, 303, 351).”
Wu, H., Huang, H., & Zhao, Y. (2023) · Frontiers in Immunology · doi:10.3389/fimmu.2023.1211221 · Cited by 103
“mTOR activates HIF-1a and Myc to enhance glycolysis, glutaminolysis, and PPP (Figure 1) (5).”
BackgroundInfluentialGlutamine addiction in tumor cell: oncogene regulation and clinical treatment
Li, X., Peng, X., Li, Y., Wei, S., He, G., Liu, J., Li, X., Yang, S., Dai, L., Lin, W., et al. (2024) · Cell Communication and Signaling · doi:10.1186/s12964-023-01449-x · Cited by 103
Nutrients: Signal 4 in T cell immunity
Raynor, J. L., & Chi, H. (2024) · The Journal of Experimental Medicine · doi:10.1084/jem.20221839 · Cited by 99
“The uptake and metabolism of glucose are required for T cell activation (Jacobs et al., 2008; Wang et al., 2011), which are coor-dinately regulated (Chapman et al., 2020).”
BackgroundSelf-citationModulation of let-7 miRNAs controls the differentiation of effector CD8 T cells
Wells, A. C., Daniels, K. A., Angelou, C. C., Fagerberg, E., Burnside, A., Markstein, M., Alfandari, D., Welsh, R. M., Pobezinskaya, E. L., & Pobezinsky, L. A. (2017) · eLife · doi:10.7554/elife.26398 · Cited by 93
“…an impact on the metabolic switch in activated CD8 T cells through its regulation of Myc, we assessed the expression of key glucose trans- porters, glycolytic enzymes, and protein synthesis enzymes that have been established as direct tar- gets of Myc in activated CD8 T cells (Wang et al., 2011).”
BackgroundInfluentialWilliamson, M. K., Coombes, N. S., Juszczak, F., Athanasopoulos, M., Khan, M. M., Eykyn, T. R., Srenathan, U., Taams, L. S., Zeidler, J. D., Poian, A. T. D., et al. (2018) · Viruses · doi:10.3390/v10030114 · Cited by 98
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Zhu, Y.-H., Zheng, J.-H., Jia, Q.-Y., Duan, Z., Yao, H., Yang, J., Sun, Y., Jiang, S.-H., Liu, D., & Huo, Y. (2022) · Cellular Oncology · doi:10.1007/s13402-022-00741-1 · Cited by 98
Impact of T cell characteristics on CAR-T cell therapy in hematological malignancies
Tao, Z., Chyra, Z., Kotulová, J., Celichowski, P., Mihályová, J., Charvátová, S., & Hájek, R. (2024) · Blood Cancer Journal · doi:10.1038/s41408-024-01193-6 · Cited by 101
“T N primarily have slow glycolysis and mainly rely on oxidative phosphorylation (OXPHOS) and fatty acid oxidation, but undergo a metabolic shift from OXPHOS to aerobic glycolysis as they become T EFF [107 – 110].”
Metabolic reprogramming in tumors: Contributions of the tumor microenvironment
Lane, A. N., Higashi, R. M., & Fan, T. W.-M. (2020) · Genes & Diseases · doi:10.1016/j.gendis.2019.10.007 · Cited by 91
The Mucosal Immune System and Its Regulation by Autophagy
Kabat, A. M., Pott, J., & Maloy, K. J. (2016) · Frontiers in Immunology · doi:10.3389/fimmu.2016.00240 · Cited by 95
Metadata
- Authors
- Wang, R., Dillon, C. P., Shi, L. Z., Milasta, S., Carter, R., Finkelstein, D., McCormick, L. L., Fitzgerald, P., Chi, H., Munger, J., & Green, D. R.
- Affiliations
- St. Jude Children's Research Hospital (US)
- University of Rochester Medicine (US)
- Corresponding author
- Green, Douglas R.
- ORCID
- Venue
- Immunity
- Publisher
- Elsevier BV
- Published
- 2011-12
- Volume
- 35
- Issue
- 6
- Pages
- 871-882
- ISSN
- 1074-7613 (ISSN-L)
- PMC
- PMC3248798
- OpenAlex
- W2079999658
- Cited by
- 2,140
- References
- 59
- Citations by year
- 2026: 137 · 2025: 147 · 2024: 168 · 2023: 175 · 2022: 220 · 2021: 203 · 2020: 199 · 2019: 173 · 2018: 158 · 2017: 150 · 2016: 127 · 2015: 99 · 2014: 80 · 2013: 62 · 2012: 37
- FWCI
- 19.59
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Immunity (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- U.S. Public Health Service (S064599)
- National Institute of General Medical Sciences (R37GM052735, R01GM052735, GM-52735)
- National Institute of Allergy and Infectious Diseases (R01AI040646, R56AI081773, AI081773, R01AI081773, AI40646)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (K01AR053573, AR053573)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Keywords
- c-Myc, T cell activation, metabolic reprogramming, glycolysis, glutaminolysis, polyamine biosynthesis, HIF-1α, TCA cycle, pentose phosphate pathway, glutamine deprivation, nucleotides, T cell proliferation, transcription factors
- MeSH terms
- Animals, Gene Expression Regulation, Glucose, Glutamine, Lymphocyte Activation, Mice, Inbred C57BL, Ornithine, Polyamines, T-Lymphocytes, Proto-Oncogene Proteins c-myc, Mice, Knockout, Mice, Hypoxia-Inducible Factor 1, alpha Subunit, Metabolic Networks and Pathways, TOR Serine-Threonine Kinases, Transcriptome
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