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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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“Because a-KG is required to maintain cell viability and minimal cell proliferation in the absence of glutamine (Wise et al., 2008), addition of a-KG alone was sufficient to drive only one cell division in the absence of glutamine.”
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“It has been shown that activated T cells have a dramatic demand for GLN as an energy and biosynthetic precursor, and GLN catabolism (glutaminolysis) is essential for T-cell proliferation in vitro and in vivo.(39) GLN-associated redox-based reactions are thought to be partly responsible for promoting T-cell proliferati…”
BackgroundGlutamine supplementation suppresses herpes simplex virus reactivation
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“In activated primary T lymphocytes, Myc drives metabolic reprogramming via a pathway of Myc-dependent metabolism, which links glutaminolysis to the biosynthesis of polyamines.(39,40) However, Myc may induce an antiinflammatory response as well, via macrophage function.”
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“through its downstream targets hypoxia inducible factor-1a (HIF1a) and Myc.(13,14) Moreover, mTORC1 can inhibit fatty acid (FA) oxidation, by”
BackgroundSelf-citationLi, C., Chiu, Y., Chang, C., Chang, Y. I., Sheu, J. J., & Chiang, A. (2021) · Cancers · doi:10.3390/cancers13133125 · Cited by 41
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BackgroundImmunometabolism shapes B cell fate and functions
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NetBID2 provides comprehensive hidden driver analysis
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“To evaluate the performance of NetBID2, we curated eight positive con-trol drivers ( Cox10 , Shmt1 , Shmt2 , Myc , Atf3 , Gabpa , Akt1 , and Gsk3b ) that had previously been identi fi ed with experimental validations 31 – 35 (Table S2).”
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“In this study, we evaluated the therapeutic effect of GLS antagonist JHU083 in ConA-induced AIH mice model, which was caused by a T cell-mediated autoimmune response (29).”
MethodBiological Aging in People Living with HIV on Successful Antiretroviral Therapy: Do They Age Faster?
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“…cells to convert glucose into pyruvate; the excess intermediate metabolites and lactate are exported by MCT1, which is activated by Myc [273,276]. c-Myc regulates the PPP’s oxidative and non-oxidative branch phases by increasing the expression of G6PDH and TKT, respectively [268] (Figure 3).”
BackgroundHensler, M., Vančurová, I., Becht, É., Palata, O., Strnad, P., Tesařová, P., Čabiňaková, M., Švec, D., Kubista, M., Bartůňková, J., et al. (2015) · OncoImmunology · doi:10.1080/2162402x.2015.1102827 · Cited by 41
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Inflammation research sails through the sea of immunology to reach immunometabolism
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“C‐myc is another important regulator of glucose uptake and T cell metabolism [53,54].”
BackgroundMetabolic Reprogramming in CD8+ T Cells During Acute Viral Infections
Gupta, S. S., Wang, J., & Chen, M. (2020) · Frontiers in Immunology · doi:10.3389/fimmu.2020.01013 · Cited by 38
“mTOR activation further leads to expression of MYC and HIF1α (15, 38), which control expression of cell cycle progression genes (cyclin A, CDK2/4, cdc25a) (11)”
BackgroundTargeting Glycolysis in Macrophages Confers Protection Against Pancreatic Ductal Adenocarcinoma
Penny, H. L., Sieow, J. L., Gun, S. Y., Lau, M. C., Lee, B. T. K., Tan, J., Phua, C., Toh, F., Nga, Y., Yeap, W. H., et al. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22126350 · Cited by 39
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“The pathway and its downstream targets HIF1-α and c-MYC are intimately involved in the regulation of cellular energetic and biosynthetic metabolism [43, 50, 57].”
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BackgroundMevalonate Metabolism in Cancer Stemness and Trained Immunity
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“GATA-3 robustly upregulates Myc (63), which drives the metabolic reprogramming associated with EMT.”
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“Wang et al. (127), reported the antigen activation of T lymphocytes drove the upregulation of genes encoding enzymes and transporters involved in glycolysis and glutaminolysis as governed by MYC.”
BackgroundImmunometabolism of Tregs: mechanisms, adaptability, and therapeutic implications in diseases
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“T cell proliferation also relies on increased glucose and glutamine metabolism.(26,29) Accordingly, antigen recognition by TCRs promotes both glucose and glutamine uptake, which in turn facilitates rapid proliferation of T cells and their activation.”
BackgroundModulating Iron for Metabolic Support of TB Host Defense
Phelan, J. J., Basdeo, S. A., Tazoll, S. C., McGivern, S., Saborido, J. R., & Keane, J. (2018) · Frontiers in Immunology · doi:10.3389/fimmu.2018.02296 · Cited by 37
“Myc upregulates various genes involved in glucose and glutamine metabolism in the initial stages of T cell activation in primary murine cells (69).”
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“MYC plays an important role in the self-renewal and differentiation of hematopoietic stem cells [27] as well as in the development of B and T lymphocytes [28,29].”
BackgroundPanda, S. K., Kim, D., Desai, P., Rodrigues, P. F., Sudan, R., Gilfillan, S., Cella, M., Dyken, S. J. V., & Colonna, M. (2022) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2215528119 · Cited by 37
Regulatory T cells suppress CD4+ effector T cell activation by controlling protein synthesis
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“This is especially true for the first 24 h prior to the onset of Teff proliferation, when the biosynthetic capacity of the cell is greatly expanded (So et al., 2016; Wang et al., 2011).”
Amino Acids Fuel T Cell-Mediated Inflammation
Poffenberger, M. C., & Jones, R. G. (2014) · Immunity · doi:10.1016/j.immuni.2014.04.017 · Cited by 38
“Of particular relevance to T cell biology is the nonessential amino acid (NEAA) glutamine, which is rapidly taken up by T cells upon activation (Carr et al., 2010; Wang et al., 2011).”
BackgroundManivannan, S., Baxter, V. K., Schultz, K. L. W., Slusher, B. S., & Griffin, D. E. (2016) · Journal of Virology · doi:10.1128/jvi.01045-16 · Cited by 36
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“Given that activated T cells upregulate amino acid transporters [14], glutamine metabolizing enzymes [15,37] as well as glutamine uptake [37,38], it is not surprisingly to observe that BPTES-treated mice display lower numbers of splenic CD4 and CD8 T cells, which pinpoints an essential role for glutamine metabolism du…”
BackgroundMetabolic signatures of immune cells in chronic kidney disease
Li, J., Yang, Y., Wang, Y., Li, Q., & He, F. (2022) · Expert Reviews in Molecular Medicine · doi:10.1017/erm.2022.35 · Cited by 36
Immunometabolic reprogramming, another cancer hallmark
Kumar, V., & Stewart, J. H. (2023) · Frontiers in Immunology · doi:10.3389/fimmu.2023.1125874 · Cited by 37
Effect of metabolic reprogramming on the immune microenvironment in gastric cancer
Shang, Z., Ma, Z., Wu, E., Chen, X., Tuo, B., Li, T., & Liu, X. (2023) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2023.116030 · Cited by 36
Targeting tumor metabolism to augment CD8+ T cell anti-tumor immunity
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“Gln can be converted into glutamate by glutaminase (GLS), and glutamate can then enter the TCA cycle after being catalyzed to a -ketoglutaric acid ( a -KG) by Gln dehydrogenase 1 (GLUD1) [85].”
Survival of the fittest: Cancer challenges T cell metabolism
Franchina, D. G., HeFeng, F. Q., & Brenner, D. (2017) · Cancer Letters · doi:10.1016/j.canlet.2017.10.014 · Cited by 34
Mu, Q., Jiang, M., Zhang, Y., Wu, F., Li, H. Z., Zhang, W., Wang, F., Liu, J., Li, L., Wang, D., et al. (2018) · OncoTargets and Therapy · doi:10.2147/ott.s154853 · Cited by 36
Early-life undernutrition reprograms CD4+ T-cell glycolysis and epigenetics to facilitate asthma
Chen, X., Lin, H., Yang, D., Xu, W., Liu, G., Liu, X., Sheng, J., & Huang, H. (2019) · Journal of Allergy and Clinical Immunology · doi:10.1016/j.jaci.2018.12.999 · Cited by 35
Metabolism and Autoimmune Responses: The microRNA Connection
Colamatteo, A., Micillo, T., Bruzzaniti, S., Fusco, C., Garavelli, S., Rosa, V. D., Galgani, M., Spagnuolo, M. I., Rella, F. D., Puca, A. A., et al. (2019) · Frontiers in Immunology · doi:10.3389/fimmu.2019.01969 · Cited by 38
Phosphoenolpyruvate from Glycolysis and PEPCK Regulate Cancer Cell Fate by Altering Cytosolic Ca2+
Moreno-Felici, J., Hyroššová, P., Aragó, M., Rodríguez‐Arévalo, S., García-Rovés, P. M., Escolano, C., & Perales, J. C. (2019) · Cells · doi:10.3390/cells9010018 · Cited by 36
BCG Vaccinations Upregulate Myc, a Central Switch for Improved Glucose Metabolism in Diabetes
Kühtreiber, W. M., Takahashi, H., Keefe, R. C., Song, Y., Tran, L., Luck, T. G., Shpilsky, G. F., Moore, L., Sinton, S. M., Graham, J. C., et al. (2020) · iScience · doi:10.1016/j.isci.2020.101085 · Cited by 37
The Ups and Downs of Metabolism during the Lifespan of a T Cell
Balyan, R., Gautam, N., & Gascoigne, N. R. J. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21217972 · Cited by 36
“In T cells, c-myc expression is induced upon activation and promotes cell growth and entry into the cell cycle [55].”
BackgroundMethodE3 ligase FBXW7 restricts M2-like tumor-associated macrophage polarization by targeting c-Myc
Zhong, L., Zhang, Y., Li, M., Song, Y., Liu, D., Yang, X., Yang, D., Qu, H., Lai, L., Wang, Q., et al. (2020) · Aging · doi:10.18632/aging.202293 · Cited by 35
Ma, C., Hoffmann, F. W., Marciel, M. P., Page, K. E., Williams-Aduja, M. A., Akana, E. N. L., Gojanovich, G. S., Gerschenson, M., Urschitz, J., Moisyadi, S., et al. (2021) · Molecular Metabolism · doi:10.1016/j.molmet.2021.101170 · Cited by 33
“TCR activation induces de novo synthesis of proteins, nucleic acids, and fatty acids accompanied by a doubling of cell sizes [30,48].”
BackgroundImmunometabolism at the Nexus of Cancer Therapeutic Efficacy and Resistance
Traba, J., Sack, M. N., Waldmann, T. A., & Antón, O. M. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2021.657293 · Cited by 39
“In these cells, even in the presence of oxygen, pyruvate is not used by the TCA cycle, but instead converted to lactate by lactate dehydrogenase A (LDHA).”
BackgroundInfluentialImmunometabolism: Towards a Better Understanding the Mechanism of Parasitic Infection and Immunity
Chen, J.-Y., Zhou, J., & Pan, W. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2021.661241 · Cited by 40
“Gln can be partially replaced by nucleotides and polyamines (102), implicating Gln as an important source for biosynthetic precursors in active T cells.”
BackgroundThe Basally Expressed p53-Mediated Homeostatic Function
Nagpal, I., & Yuan, Z.-M. (2021) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2021.775312 · Cited by 35
“Wang et al. demonstrated that metabolic reprogramming from the TCA cycle to the anabolic pathways, including glycolysis, pentosephosphate, and glutaminolysis, is coupled with T cell activation (Wang et al., 2011).”
BackgroundInfluentialWells, A. C., Hioki, K. A., Angelou, C. C., Lynch, A. C., Liang, X., Ryan, D. J., Thesmar, I., Zhanybekova, S., Žuklys, S., Ullom, J., et al. (2023) · Nature Communications · doi:10.1038/s41467-023-40959-7 · Cited by 35
“3e), suggesting that let-7 further supports differentiation of the memory lineage by restricting glycolysis 62 – 64 .”
Edmunds, L. R., Sharma, L., Wang, H., Kang, A., D'Souza, S. S., Lu, J. L., McLaughlin, M., Dolezal, J. M., Gao, X., Weintraub, S. T., et al. (2015) · PLoS ONE · doi:10.1371/journal.pone.0134049 · Cited by 35
“This has the effect of increasing the production of ATP needed to support macromolecular synthesis during proliferation [15, 20, 22].”
BackgroundArciuch, V. G. A., Russo, M. A., Kang, K. S., & Cristofano, A. D. (2013) · Cancer Research · doi:10.1158/0008-5472.can-13-1429 · Cited by 38
“Although an elegant study has recently established that activated lymphocytes rely mainly on MYC to transcriptionally reprogram their metabolism (38), much less is known when it comes to epithelial cells.”
Metabolic Factors that Contribute to Lupus Pathogenesis
Li, W., Sivakumar, R., Titov, A. A., Choi, S., & Morel, L. M. (2016) · Critical Reviews in Immunology · doi:10.1615/critrevimmunol.2016017164 · Cited by 35
Jantz-Naeem, N., Loschinski, R., Borucki, K., Mitchell-Flack, M., Böttcher, M., Schraven, B. L., Mougiakakos, D., & Kahlfuß, S. (2023) · Frontiers in Oncology · doi:10.3389/fonc.2023.1060112 · Cited by 37
“Frontiers in Oncology 02 activation (28), mTOR induces the increased expression of glucose transporter 1 (GLUT1) and CD98, a protein responsible for transporting amino acids into the cell (29).”
BackgroundFu, J., Huang, S.-J., Wang, B., Yin, J., Chen, C.-Y., Xu, J., Chen, Y., Xu, S., Dong, T., Zhou, H., et al. (2024) · Cell Metabolism · doi:10.1016/j.cmet.2023.12.016 · Cited by 33
Wüstner, S., Mejías‐Luque, R., Koch, M. F., Rath, E., Vieth, M. W., Sieber, S. A., Haller, D., & Gerhard, M. (2014) · Cellular Microbiology · doi:10.1111/cmi.12335 · Cited by 37
“Furthermore, we show that cMyc induction, upon T-cell stimulation, was compromised in presence of H. pylori gGT. cMyc is responsible for expression of enzymes required for glutaminolysis and increased glutamine uptake upon T-cell activation (Wang et al., 2011).”
BackgroundInfluentialRashkovan, M., Vadnais, C., Ross, J., Gigoux, M., Suh, W., Gu, W. J., Kosan, C., & Möröy, T. (2014) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1412107111 · Cited by 34
“In addition, CD71 and CD98, key metabolic genes up-regulated at the DNto-DP transition and direct targets of c-Myc (33, 34), are not upregulated on Rag1 × Miz-1 DN4 cells after mitogenic stimulation.”
BackgroundMetal oxide nanoparticles interact with immune cells and activate different cellular responses
Simón‐Vázquez, R., Lozano‐Fernández, T., Dávila-Grana, Á., & González‐Fernández, Á. (2016) · International Journal of Nanomedicine · doi:10.2147/ijn.s110465 · Cited by 34
“Activated T cells undergo some metabolic changes common to tumor cells and this may represent a general metabolic reprogramming during cell growth and proliferation.(35,36) Moreover, upregulation of the IL-2 and BCL2A1 genes is also associated with lymphocyte activation.”
BackgroundTargeting T Cell Metabolism in Inflammatory Skin Disease
von Meyenn, L., Bertschi, N., & Schlapbach, C. (2019) · Frontiers in Immunology · doi:10.3389/fimmu.2019.02285 · Cited by 32
“Effector TH cells and CD8 T cells show increased glycolytic activity as compared to naive T cells (16, 67), but not all TH cell lineages have equal glucose metabolism signatures.”
BackgroundRezinciuc, S., Bezavada, L., Bahadoran, A., Duan, S., Wang, R., López‐Ferrer, D., Zink, E. E., Finklestein, D., Green, D. R., Paša‐Tolić, L., et al. (2020) · PLoS Pathogens · doi:10.1371/journal.ppat.1008957 · Cited by 35
“To validate the protein network analysis and further characterize influenza-induced changes in metabolism, we quantified glucose, pyruvate, glutamine, and palmitic acid oxidation, as previously described [14].”
BackgroundMethodInfluentialSelf-citationMetabolic profiles of regulatory T cells in the tumour microenvironment
Rao, D., Verburg, F., Renner, K., Peeper, D. S., Lacroix, R., & Blank, C. U. (2021) · Cancer Immunology Immunotherapy · doi:10.1007/s00262-021-02881-z · Cited by 43
MTOR Signaling and Metabolism in Early T Cell Development
Werlen, G., Jain, R., & Jacinto, E. (2021) · Genes · doi:10.3390/genes12050728 · Cited by 35
“Mycophenolates are converted to mycophenolic acid in the liver, and this metabolite inhibits the rate-limiting enzyme, inosine monophosphate dehydrogenase, of the de novo synthesis of guanosine nucleotides [21].”
BackgroundInfluentialProline Metabolism in Neurological and Psychiatric Disorders
Yao, Y., & Han, W. (2022) · Molecules and Cells · doi:10.14348/molcells.2022.0115 · Cited by 34
“Additional lines of evidence suggest that proline metabolism contributes to the reprogramming of tumor-infiltrating macrophages (Abuawad et al., 2020; Kuo et al., 2020; Wang et al., 2011).”
Soriano‐Baguet, L., Grusdat, M., Kurniawan, H., Benzarti, M., Binsfeld, C., Ewen, A., Longworth, J., Bonetti, L., Guerra, L., Franchina, D. G., et al. (2023) · Cell Reports · doi:10.1016/j.celrep.2023.112153 · Cited by 33
A multi‐scale approach reveals that NF‐κB cRel enforces a B‐cell decision to divide
Shokhirev, M. N., Almaden, J., Davis‐Turak, J., Birnbaum, H. A., Russell, T. M., Vargas, J. D., & Hoffmann, A. (2015) · Molecular Systems Biology · doi:10.15252/msb.20145554 · Cited by 32
“…is consistent with the observation that a subset of generation 0 cells prepare for several rounds of rapid divisions by simultaneously deactivating quiescence (Yusuf & Fruman, 2003; Hawkins et al , 2009) and activating growth pathways such as Myc and mTOR (Grumont et al , 2002; Wang et al , 2011).”
Cell Cycle Entry Control in Naïve and Memory CD8+ T Cells
Lewis, D. A., & Ly, T. (2021) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2021.727441 · Cited by 32
Immunometabolism changes in fibrosis: from mechanisms to therapeutic strategies
Feng, L., Chen, X., Huang, Y., Zhang, X., Zheng, S., & Xie, N. (2023) · Frontiers in Pharmacology · doi:10.3389/fphar.2023.1243675 · Cited by 35
“Amino acid metabolism, including glutamine, arginine, serine and glycine, is critical in T cell proliferation and differentiation (Wang et al., 2011; Kishton et al., 2016; Ma et al., 2017).”
BackgroundMitochondrial dysfunctions in T cells: focus on inflammatory bowel disease
Lee, H., Jeon, J., & Kim, E. S. (2023) · Frontiers in Immunology · doi:10.3389/fimmu.2023.1219422 · Cited by 33
“It is strongly upregulated in both CD4 + and CD8 + T cells after TCR activation (83, 84).”
InfluentialBrookens, S. K., Cho, S. H., Paik, Y., Meyer, K., Raybuck, A. L., Park, C., Greenwood, D. L., Rathmell, J. C., & Boothby, M. R. (2023) · The Journal of Immunology · doi:10.4049/jimmunol.2200756 · Cited by 37
Metabolic reprogramming of CAR T cells: a new frontier in cancer immunotherapy
Frlic, T., & Pavlin, M. (2025) · Frontiers in Immunology · doi:10.3389/fimmu.2025.1688995 · Cited by 38
“Glycolysis rapidly generates ATP and provides critical intermediates for macromolecule biosynthesis, crucial for clonal expansion and effector functions (61, 80, 83, 92, 93).”
DCAF1 controls T-cell function via p53-dependent and -independent mechanisms
Guo, Z., Kong, Q., Liu, C., Zhang, S., Zou, L., Yan, F., Whitmire, J. K., Xiong, Y., Chen, X., & Wan, Y. Y. (2016) · Nature Communications · doi:10.1038/ncomms10307 · Cited by 32
RNA-sequencing Identifies Novel Pathways in Sarcoidosis Monocytes
Talreja, J., Farshi, P., Alazizi, A., Luca, F., Piqué-Regi, R., & Samavati, L. (2017) · Scientific Reports · doi:10.1038/s41598-017-02941-4 · Cited by 33
Metabolomics in Immunology Research
Everts, B. (2018) · Methods in molecular biology · doi:10.1007/978-1-4939-7592-1_2 · Cited by 33
T-Cell Metabolism in Hematopoietic Cell Transplantation
Nguyen, H. D., Kuril, S., Bastian, D. A., & Yu, X. (2018) · Frontiers in Immunology · doi:10.3389/fimmu.2018.00176 · Cited by 34
“During activation, in vitro activated T cells augment fatty acid synthase (FAS) while decreasing FAO, thus enhancing the accumulation of FA metabolites needed for the membrane (17).”
BackgroundInfluentialImmunometabolic cross-talk in the inflamed heart
Marelli‐Berg, F. M., & Aksentijević, D. (2019) · Cell Stress · doi:10.15698/cst2019.08.194 · Cited by 36
“Of note, HIF1α is not required for the initiation of aerobic glycolysis in activated T cells; instead, c-Myc is uniquely mediating this metabolic shift [172].”
BackgroundQiu, R., Yu, X., Wang, L., Han, Z., Yao, C., Cui, Y., Hou, G., Dai, D., Jin, W., & Shen, N. (2020) · The Journal of Immunology · doi:10.4049/jimmunol.2000060 · Cited by 36
IL‐33 activates mTORC1 and modulates glycolytic metabolism in CD8+ T cells
Liang, Y., Wang, X., Wang, H., Yang, W., Yi, P., Soong, L., Cong, Y., Cai, J., Fan, X., & Sun, J. (2021) · Immunology · doi:10.1111/imm.13404 · Cited by 35
“Although the underlying mechanism of mTORC1- regulated aerobic glycolysis is not totally clear, the transcription factors cMyc and hypoxia- inducible factor 1alpha (HIF1α) have been demonstrated to be the key players in this metabolic programming [29].”
BackgroundAcsbg1 Dependent Mitochondrial Fitness is a Metabolic Checkpoint for Tissue T reg Cell Homeostasis
Kanno, T., Nakajima, T., Kawashima, Y., Yokoyama, S., Asou, H. K., Sasamoto, S., Hayashizaki, K., Kinjo, Y., Ohara, O., Nakayama, T., et al. (2021) · Cell Reports · doi:10.1016/j.celrep.2021.109921 · Cited by 35
Anatskaya, O. V., & Vinogradov, A. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23179691 · Cited by 27
Rapamycin Suppresses Tumor Growth and Alters the Metabolic Phenotype in T-Cell Lymphoma
Kittipongdaja, W., Wu, X., Garner, J. A., Liu, X., Komas, S. M., Hwang, S. T., & Schieke, S. M. (2015) · Journal of Investigative Dermatology · doi:10.1038/jid.2015.153 · Cited by 34
Niu, N., Ye, J., Hu, Z., Zhang, J., & Wang, Y. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24087076 · Cited by 34
Brescia, C., Audia, S., Pugliano, A., Scaglione, F., Iuliano, R., Trapasso, F., Perrotti, N., Chiarella, E., & Amato, R. (2024) · Apmis · doi:10.1111/apm.13378 · Cited by 34
“Memory T cells use extra mechanisms like NOTCH signaling to enhance AKT activation, GLUT1 expression, and glucose absorption [179] which produce and accumulate essential lipids, AA, and nucleic acids for cell expansion [148].”
The global role of G6PD in infection and immunity
Shah, S. S., Stone, E. F., Francis, R. O., & Karafin, M. S. (2024) · Frontiers in Immunology · doi:10.3389/fimmu.2024.1393213 · Cited by 32
“In particular, ROS affects T cell receptor signaling through several downstream signaling pathways (57, 61, 62), including mitogen-activated protein kinase (MAPK), phosphoinositide 3-kinases (PI3K), and Janus kinase-signal transducer and activator of transcription 3 (JAK-STAT3).”
BackgroundTargeting amino acid-metabolizing enzymes for cancer immunotherapy
Grobben, Y. (2024) · Frontiers in Immunology · doi:10.3389/fimmu.2024.1440269 · Cited by 35
“Accordingly, glutamine-depriving conditions compromise the growth and proliferation of activated T cells in vitro (79, 80), whereas restoration of tumor interstitial glutamine levels by tumor-speci fi c GLS1 knockout increases T-cell in fi ltration and activity in vivo (Figure 4B) (38).”
BackgroundPotter, M. C., Baxter, V. K., Mathey, R. W., Alt, J., Rojas, C., Griffin, D. E., & Slusher, B. S. (2015) · Journal of NeuroVirology · doi:10.1007/s13365-015-0314-6 · Cited by 32
“…administration of a glutamine antagonist, DON, which affects two different mechanisms known to contribute to the pathology seen during SINV infection: inflammatory damage induced by the immune response and glutamate excitotoxicity (Newsholme et al. 1985; Greene et al. 2008; Wang et al. 2011).”
BackgroundInfluential
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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