ArticleCell metabolism2022
The glucose transporter GLUT3 controls T helper 17 cell responses through glycolytic-epigenetic reprogramming.
Article in Cell metabolism, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 148 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
148 citing papers in PubMed, 221 citations in OpenAlex.
- The SLC-ome of membrane transport: from molecular discovery to physiology and clinical applications.Physiological reviews · 2026Review
- CB2 Receptor Activation Attenuates IL-1β-Induced Inflammatory Transcriptomic Networks in Human Gingival Fibroblasts.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Review
- Unconventional role of hydroxymethylglutaryl-CoA synthase 1 in driving pathogenic TScience advances · 2026Article
- An epigenetic switch in β-cells links mitochondrial stress to inflammatory fate via HMGB1 acetylation.Cell death and differentiation · 2026Article
- Vitamin B5 supports anti-PD1 response in HER2-positive gastric cancer and enhances interaction between naïve B cells and T cells.Nature communications · 2026Article
- Mitochondrial Metabolic Reprogramming and Skin Immune Homeostasis: From Basic Mechanisms to Therapeutic Perspectives.Immune network · 2026Review
- High Glucose Supplementation Aggravates Experimental Autoimmune Epididymo-orchitis via Localized Th17 Skewing in the Male Reproductive Tract.American journal of reproductive immunology (New York, N.Y. : 1989) · 2026Article
- The Glucose Transporter GLUT3 Controls Regulatory T Cell Function.European journal of immunology · 2026Article
- Panax notoginseng saponins (PNS)alleviates rheumatoid arthritis by regulating HIF-1α/PKM2-mediated glycolysis to inhibit Th17 differentiation.Molecular biology reports · 2026Article
- ISL@mTOMV nanoparticles: a promising approach for VM-targeted therapy in breast cancer.Journal of nanobiotechnology · 2026Article
- High-Glucose-Induced Metabolic and Epithelial Stress in Grass Carp Intestinal Epithelial Cells Associated with Methylation-Related Transcriptional Responses.International journal of molecular sciences · 2026Article
- Mitochondrial OXPHOS restricts SARS-CoV-2 replication.Science advances · 2026Article
- The role of tumor metabolic reprogramming in acquired anti-PD-1/PD-L1 resistance.Translational lung cancer research · 2026Review
- ACLY integrates metabolism and chromatin accessibility to enable B Cell activation and humoral immunity.bioRxiv : the preprint server for biology · 2026Article
- Two Faces of NFAT Transcription Factors in LymphocytesBiomolecules · 2026Review
- Solute carrier transporters as metabolic gatekeepers in tumor-microenvironment crosstalk.Acta pharmacologica Sinica · 2026Review
- Metabolic modulation of immune cell function: mechanisms and therapeutic implications in cancer immunotherapy.Oncogenesis · 2026Review
- Contextualizing TNature reviews. Immunology · 2026Review
- Metabolic reprogramming of Th17/Treg imbalance in autoimmune thyroid diseases.Cell communication and signaling : CCS · 2026Review
88 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
Authors and funding
16 authors at 6 institutions in 4 countries.
Funding
Abstract
Metabolic reprogramming is a hallmark of activated T cells. The switch from oxidative phosphorylation to aerobic glycolysis provides energy and intermediary metabolites for the biosynthesis of macromolecules to support clonal expansion and effector function. Here, we show that glycolytic reprogramming additionally controls inflammatory gene expression via epigenetic remodeling. We found that the glucose transporter GLUT3 is essential for the effector functions of Th17 cells in models of autoimmune colitis and encephalomyelitis. At the molecular level, we show that GLUT3-dependent glucose uptake controls a metabolic-transcriptional circuit that regulates the pathogenicity of Th17 cells. Metabolomic, epigenetic, and transcriptomic analyses linked GLUT3 to mitochondrial glucose oxidation and ACLY-dependent acetyl-CoA generation as a rate-limiting step in the epigenetic regulation of inflammatory gene expression. Our findings are also important from a translational perspective because inhibiting GLUT3-dependent acetyl-CoA generation is a promising metabolic checkpoint to mitigate Th17-cell-mediated inflammatory diseases.
Indexed as
Identifiers
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.