ArticleCell2020
Niche-Selective Inhibition of Pathogenic Th17 Cells by Targeting Metabolic Redundancy.
Article in Cell, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers, 1 of them a synthesis that pooled it.
What it found
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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
81 citing papers in PubMed, 1 synthesis or guideline pooled it.
- CRISPR and Myelin regeneration: a systematic review of applications in demyelinating CNS Disorders, with a focus on MS.Regenerative medicine · 2025Pooled it
- Metabolic determinants of autoimmune kidney diseases.Nature reviews. Nephrology · 2026Review
- Metabolic switch: lymphocytes and the onset of T-cell-mediated autoimmunity.Cellular & molecular immunology · 2026Review
- Panax notoginseng saponins (PNS)alleviates rheumatoid arthritis by regulating HIF-1α/PKM2-mediated glycolysis to inhibit Th17 differentiation.Molecular biology reports · 2026Article
- HIV-1 Nef generates lasting innate immune memory in haematopoietic stem and progenitor cells in vivo.EMBO reports · 2026Article
- Immunosenescence in systemic and multi-organ aging: mechanisms, inter-organ crosstalk, and translational opportunities.npj aging · 2026Review
- Contextualizing TNature reviews. Immunology · 2026Review
- Resident microbes shape host immunity and protect against pathogen infection and inflammatory disease.Cellular and molecular life sciences : CMLS · 2026Review
- Metabolic reprogramming of Th17/Treg imbalance in autoimmune thyroid diseases.Cell communication and signaling : CCS · 2026Review
- Tissue-restricted secondary TCR engagement drives the transition from stem-like to CD200Nature immunology · 2026Article
- Enhanced HIF-1α cooperation by a human RORγt mutant potentiates Th17 pathogenicity.Cell reports · 2026Article
- TPP-Thiazole Derivatives Ameliorate Psoriasiform Inflammation by Glycolysis Inhibition.Molecules (Basel, Switzerland) · 2026Article
- Pyruvate kinase muscle 2 (PKM2) promotes CD4 T cell survival by regulating pyruvate oxidation during homeostasis and expansion.Science advances · 2026Article
- A thermosensitive hydrogel encapsulating 2-DG alleviates periodontitis by inhibiting glycolysis and effector response of Th17 cells.Frontiers in pharmacology · 2026Article
- Oxidative pentose phosphate pathway is required for T cell activation and antitumor immunity.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Fructose intake driven glycolysis-ROS-EGFR axis specifically promotes the generation and pathogenicity of Th17 cells.Nature communications · 2025Article
- Regulation of CD4 + T cell differentiation and function by glucose metabolism.Genes and immunity · 2025Review
- The glycolytic reaction PGAM restrains Th17 pathogenicity and Th17-dependent autoimmunity.Cell reports · 2025Article
- Targeting CD38 immunometabolic checkpoint improves metabolic fitness and cognition in a mouse model of Alzheimer's disease.Nature communications · 2025Article
- Metabolic reprogram and T cell differentiation in inflammation: current evidence and future perspectives.Cell death discovery · 2025Review
21 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on byT2020
Authors and funding
17 authors.
Funding
Abstract
Targeting glycolysis has been considered therapeutically intractable owing to its essential housekeeping role. However, the context-dependent requirement for individual glycolytic steps has not been fully explored. We show that CRISPR-mediated targeting of glycolysis in T cells in mice results in global loss of Th17 cells, whereas deficiency of the glycolytic enzyme glucose phosphate isomerase (Gpi1) selectively eliminates inflammatory encephalitogenic and colitogenic Th17 cells, without substantially affecting homeostatic microbiota-specific Th17 cells. In homeostatic Th17 cells, partial blockade of glycolysis upon Gpi1 inactivation was compensated by pentose phosphate pathway flux and increased mitochondrial respiration. In contrast, inflammatory Th17 cells experience a hypoxic microenvironment known to limit mitochondrial respiration, which is incompatible with loss of Gpi1. Our study suggests that inhibiting glycolysis by targeting Gpi1 could be an effective therapeutic strategy with minimum toxicity for Th17-mediated autoimmune diseases, and, more generally, that metabolic redundancies can be exploited for selective targeting of disease processes.
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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.