ArticleScience translational medicine2015
Normalization of CD4+ T cell metabolism reverses lupus.
Article in Science translational medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 385 papers.
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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.
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Who cites it
385 citing papers in PubMed, 589 citations in OpenAlex.
- Biologic Mechanisms Underlying the Heterogeneous Response to Tight Glycemic Control among Differentially Inflamed Patients in the HALF-PINT Trial.American journal of respiratory and critical care medicine · 2025Trial
- Circulating miR-320b Contributes to CD4+ T-Cell Proliferation in Systemic Lupus Erythematosus via MAP3K1.Journal of immunology research · 2023Trial
- Safety and efficacy of the SGLT2 inhibitor dapagliflozin in patients with systemic lupus erythematosus: a phase I/II trial.RMD open · 2022Trial
- Dimethyl fumarate treatment restrains the antioxidative capacity of T cells to control autoimmunity.Brain : a journal of neurology · 2021Trial
- Immunometabolism and rheumatic disease-advancing targeted therapies.EULAR rheumatology open · 2026Review
- Metabolic switch: lymphocytes and the onset of T-cell-mediated autoimmunity.Cellular & molecular immunology · 2026Review
- Metabolic determinants of autoimmune kidney diseases.Nature reviews. Nephrology · 2026Review
- Targeting tissue immune memory in chronic-remitting autoimmune kidney diseases: current concepts and future therapies.Clinical kidney journal · 2026Review
- Gut metaproteomics reveals activated arginine catabolism and impaired arginine biosynthesis in systemic lupus erythematosus.mSystems · 2026Article
- Shared Major Metabolic Pathways and Potential Targeted Therapies in Malignancies and Systemic Lupus Erythematosus.Biomolecules · 2026Review
- Upregulated GLUT1 expression correlates with type I interferon activity and disease severity in cutaneous lupus erythematosus.Journal of translational autoimmunity · 2026Article
- From Genes to Pathways: The Molecular Landscape of Systemic Lupus Erythematosus.International journal of molecular sciences · 2026Review
- Cells' survival pattern of kidney macrophages and epithelial cells in lupus nephritis is influenced by glycolysis.Lupus science & medicine · 2026Article
- Multiomics-guided discovery of protective microbiome signatures in lupus-prone mice treated with Faecalibacterium prausnitzii.Nature communications · 2026Article
- Glucose metabolic reprogramming in systemic lupus erythematosus and lupus nephritis: theoretical foundations and therapeutic implications.Frontiers in immunology · 2026Review
- Accelerated immunosenescence in SLE: current evidence and clinical translation.Frontiers in immunology · 2026Review
- The landscape of cellular immune alteration in systemic lupus erythematosus.Frontiers in immunology · 2026Review
- Systemic lupus erythematosus-driven accelerated atherosclerosis: the immune-metabolic-vascular axis and therapeutic implications.Frontiers in immunology · 2026Review
- Glycolysis inhibition functionally reprograms T follicular helper cells and reverses lupus.Cell reports · 2025Article
- Glomerular endothelial cells eliminate nicotinamide adenine dinucleotide to instruct CD103Proceedings of the National Academy of Sciences of the United States of America · 2025Article
325 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Systemic lupus erythematosus (SLE) is an autoimmune disease in which autoreactive CD4(+) T cells play an essential role. CD4(+) T cells rely on glycolysis for inflammatory effector functions, but recent studies have shown that mitochondrial metabolism supports their chronic activation. How these processes contribute to lupus is unclear. We show that both glycolysis and mitochondrial oxidative metabolism are elevated in CD4(+) T cells from lupus-prone B6.Sle1.Sle2.Sle3 (TC) mice as compared to non-autoimmune controls. In vitro, both the mitochondrial metabolism inhibitor metformin and the glucose metabolism inhibitor 2-deoxy-d-glucose (2DG) reduced interferon-γ (IFN-γ) production, although at different stages of activation. Metformin also restored the defective interleukin-2 (IL-2) production by TC CD4(+) T cells. In vivo, treatment of TC mice and other lupus models with a combination of metformin and 2DG normalized T cell metabolism and reversed disease biomarkers. Further, CD4(+) T cells from SLE patients also exhibited enhanced glycolysis and mitochondrial metabolism that correlated with their activation status, and their excessive IFN-γ production was significantly reduced by metformin in vitro. These results suggest that normalization of T cell metabolism through the dual inhibition of glycolysis and mitochondrial metabolism is a promising therapeutic venue for SLE.
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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.