ArticleEuropean journal of immunology2016
Leptin directly promotes T-cell glycolytic metabolism to drive effector T-cell differentiation in a mouse model of autoimmunity.
Article in European journal of immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers, 2 of them syntheses 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.
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Who cites it
79 citing papers in PubMed, 2 syntheses or guidelines pooled it, 155 citations in OpenAlex.
- A systematic review on leptin's role in defining cancer: special emphasis on immunomodulation, inflammation, and therapeutic interventions.Genes and immunity · 2025Pooled it
- Predictive value of adipokines for the severity of acute pancreatitis: a meta-analysis.BMC gastroenterology · 2024Pooled it
- Immunoregulation induced by autologous serum collected after acute exercise in obese men: a randomized cross-over trial.Scientific reports · 2020Trial
- Hidradenitis suppurativa: epidemiology, diagnosis, molecular pathogenesis and therapy.Molecular biomedicine · 2026Review
- Context-specific regulatory genetic variation in MTOR dampens neutrophil-T cell crosstalk in pneumonia-associated sepsis.Nature communications · 2026Article
- The mechanistic role of adipokine imbalance in airway inflammation, hyperresponsiveness, and remodeling in obesity-related asthma.Frontiers in endocrinology · 2026Review
- Leptin as a Potential Modifier of Neuroinflammation: Contrasting Roles in Alzheimer's Disease and Multiple Sclerosis.International journal of molecular sciences · 2025Review
- An age-related decrease in leptin contributes to CD8Cell reports. Medicine · 2025Article
- Th17 cell pathogenicity in autoimmune disease.Experimental & molecular medicine · 2025Review
- Immune Dysregulation Connecting Type 2 Diabetes and Cardiovascular Complications.Life (Basel, Switzerland) · 2025Review
- Obesity: Next game changer of allergic airway diseases?Clinical and translational medicine · 2025Review
- Identification and validation of key biomarkers associated with immune and oxidative stress for preeclampsia by WGCNA and machine learning.Frontiers in genetics · 2025Article
- Th17/Treg imbalance in inflammatory bowel disease: immunological mechanisms and microbiota-driven regulation.Frontiers in immunology · 2025Review
- Impact of hyperglycemia on immune cell function: a comprehensive review.Diabetology international · 2024Review
- Immunometabolism in atherosclerotic disorders.Nature cardiovascular research · 2024Review
- Emerging mechanisms of obesity-associated immune dysfunction.Nature reviews. Endocrinology · 2024Review
- Renal transcriptome analysis of uninephrectomized db/db mice identified a mechanism for the transition to severe diabetic nephropathy.Experimental animals · 2024Article
- Macrophage and T cell networks in adipose tissue.Nature reviews. Endocrinology · 2024Review
- Implications of immunometabolism for smouldering MS pathology and therapy.Nature reviews. Neurology · 2023Review
- High tissue-sodium associates with systemic inflammation and insulin resistance in obese individuals.Nutrition, metabolism, and cardiovascular diseases : NMCD · 2023Article
19 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Upon activation, T cells require energy for growth, proliferation, and function. Effector T (Teff) cells, such as Th1 and Th17 cells, utilize high levels of glycolytic metabolism to fuel proliferation and function. In contrast, Treg cells require oxidative metabolism to fuel suppressive function. It remains unknown how Teff/Treg-cell metabolism is altered when nutrients are limited and leptin levels are low. We therefore examined the role of malnutrition and associated hypoleptinemia on Teff versus Treg cells. We found that both malnutrition-associated hypoleptinemia and T cell-specific leptin receptor knockout suppressed Teff-cell number, function, and glucose metabolism, but did not alter Treg-cell metabolism or suppressive function. Using the autoimmune mouse model EAE, we confirmed that fasting-induced hypoleptinemia altered Teff-cell, but not Treg-cell, glucose metabolism, and function in vivo, leading to decreased disease severity. To explore potential mechanisms, we examined HIF-1α, a key regulator of Th17 differentiation and Teff-cell glucose metabolism, and found HIF-1α expression was decreased in T cell-specific leptin receptor knockout Th17 cells, and in Teff cells from fasted EAE mice, but was unchanged in Treg cells. Altogether, these data demonstrate a selective, cell-intrinsic requirement for leptin to upregulate glucose metabolism and maintain function in Teff, but not Treg cells.
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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.