ArticleCell2016
Mitochondrial Dynamics Controls T Cell Fate through Metabolic Programming.
Article in Cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04259372 (Analysis of T Cell Metabolism and Immune Phenotype During the Course of Acute Myeloid Leukemia), which is not on this map. Cited by 912 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Analysis of T Cell Metabolism and Immune Phenotype During the Course of Acute Myeloid Leukemia
Who cites it
912 citing papers in PubMed, 1,391 citations in OpenAlex.
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- A Multi-Targeting Chimeric Antigen Receptor-T Cell Platform to Overcome Antigen Heterogeneity in the Treatment of Non-Small Cell Lung Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Metabolic profiling of CAR T-cells in patients reveals a shift toward amino acid-supported OXPHOS and informs transporter engineering.Research square · 2026Article
- Epigenetic insights and innovations for overcoming barriers in CAR-T cell therapy for cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
- Mitochondrial Fitness as a Functional Immune Checkpoint in Cancer: Metabolic Plasticity, Tumor Evolution, and Immunotherapy.Cancers · 2026Review
- Mitochondrial dynamics and T cells immunity in cancer.Biochemistry and biophysics reports · 2026Review
- Refuel and endure: improving metabolic fitness and efficacy in CAR-T therapy.Immuno-oncology technology · 2026Article
- Microbiome-derived metabolites shape CD4+ T cell differentiation and immune aging in HIV-1 infection.JCI insight · 2026Article
- Unconventional role of hydroxymethylglutaryl-CoA synthase 1 in driving pathogenic TScience advances · 2026Article
- Genome-wide association study and predictors of neonatal blood cell traits in Hispanic newborns.American journal of human genetics · 2026Article
- Nicotinamide riboside enhances adoptive T cell therapy by promoting memory differentiation and metabolic fitness.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Organelle-specific fluorescent probes for live imaging at the nanoscale.Science China. Life sciences · 2026Review
- Mitochondrial Metabolic Reprogramming and Skin Immune Homeostasis: From Basic Mechanisms to Therapeutic Perspectives.Immune network · 2026Review
- GRP75 sustains CD8Cell death and differentiation · 2026Article
- Rewiring glucose metabolism in pancreatic cancer by natural compounds: implications for immune evasion and therapeutic targets.Molecular biology reports · 2026Review
- Review
- Cancer stem cell plasticity: mechanisms, immune microenvironment crosstalk, and therapeutic implications.Journal of hematology & oncology · 2026Review
- FAS-controlled T cells drive lymphoproliferation through glycolysis without effector differentiation.Journal of human immunity · 2026Article
852 more citing papers are in PubMed but not listed here.
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Authors and funding
19 authors at 7 institutions in 3 countries.
Funding
Abstract
Activated effector T (TE) cells augment anabolic pathways of metabolism, such as aerobic glycolysis, while memory T (TM) cells engage catabolic pathways, like fatty acid oxidation (FAO). However, signals that drive these differences remain unclear. Mitochondria are metabolic organelles that actively transform their ultrastructure. Therefore, we questioned whether mitochondrial dynamics controls T cell metabolism. We show that TE cells have punctate mitochondria, while TM cells maintain fused networks. The fusion protein Opa1 is required for TM, but not TE cells after infection, and enforcing fusion in TE cells imposes TM cell characteristics and enhances antitumor function. Our data suggest that, by altering cristae morphology, fusion in TM cells configures electron transport chain (ETC) complex associations favoring oxidative phosphorylation (OXPHOS) and FAO, while fission in TE cells leads to cristae expansion, reducing ETC efficiency and promoting aerobic glycolysis. Thus, mitochondrial remodeling is a signaling mechanism that instructs T cell metabolic programming.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.