ArticleJournal of neuroinflammation2018
Enhanced glycolysis contributes to the pathogenesis of experimental autoimmune neuritis.
Article in Journal of neuroinflammation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 60 citations in OpenAlex.
- Dynamic metabolic programming of monocyte-derived cells defines immunity in CNS disease.Brain : a journal of neurology · 2026Review
- Targeting Glycolysis May Bridge Innate and Adaptive Immune Regulation in Experimental Peri-Implantitis.International journal of molecular sciences · 2026Article
- Panax notoginseng saponins (PNS)alleviates rheumatoid arthritis by regulating HIF-1α/PKM2-mediated glycolysis to inhibit Th17 differentiation.Molecular biology reports · 2026Article
- Tomato Spotted Wilt Virus Reprogrammes Host Glycolysis to Facilitate Proliferation by a Phase-Separated Co-Aggregate of Nucleocapsid Protein and Phosphoglycerate Kinase.Plant biotechnology journal · 2026Article
- Peripheral blood T-cell subsets combined with EGRIS score predict the need for mechanical ventilation in Guillain-Barré syndrome.Frontiers in immunology · 2026Article
- Metabolic checkpoints in the regulation of Th17 cells: implications for uveitis pathogenesis and therapy.Frontiers in immunology · 2026Review
- Experimental Autoimmune Neuritis Nerve Demyelination Is Attenuated by Blocking JAK2/STAT3 Signaling Pathway in Rats.Brain and behavior · 2025Article
- Myeloid PTEN loss affects the therapeutic response by promoting stress granule assembly and impairing phagocytosis by macrophages in breast cancer.Cell death discovery · 2024Article
- Mechanical gated ion channel Piezo1: Function, and role in macrophage inflammatory response.Innate immunity · 2024Review
- Macrophage-Derived Extracellular Vesicles-Coated Palladium Nanoformulations Modulate Inflammatory and Immune Homeostasis for Targeting Therapy of Ulcerative Colitis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Methylglyoxal suppresses microglia inflammatory response through NRF2-IκBζ pathway.Redox biology · 2023Article
- Progress in Guillain-Barré syndrome immunotherapy-A narrative review of new strategies in recent years.Human vaccines & immunotherapeutics · 2023Review
- 2-DG Regulates Immune Imbalance on the Titanium Surface after Debridement.International journal of molecular sciences · 2023Article
- Iron controls T helper cell pathogenicity by promoting glucose metabolism in autoimmune myopathy.Clinical and translational medicine · 2022Article
- Helicobacter pylori-mediated gastric pathogenesis is attenuated by treatment of 2-deoxyglucose and metformin.Journal of microbiology (Seoul, Korea) · 2022Article
- Blood-based untargeted metabolomics in relapsing-remitting multiple sclerosis revealed the testable therapeutic target.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Providing a Helping Hand: Metabolic Regulation of T Follicular Helper Cells and Their Association With Disease.Frontiers in immunology · 2022Review
- A Deep Insight Into Regulatory T Cell Metabolism in Renal Disease: Facts and Perspectives.Frontiers in immunology · 2022Review
- Alcohol Impairs Immunometabolism and Promotes Naïve T Cell Differentiation to Pro-Inflammatory Th1 CD4Frontiers in immunology · 2022Article
- Ion channel Piezo1 activation promotes aerobic glycolysis in macrophages.Frontiers in immunology · 2022Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundWith the recognition of the key roles of cellular metabolism in immunity, targeting metabolic pathway becomes a new strategy for autoimmune disease treatment. Guillain-Barré syndrome (GBS) is an acute immune-mediated inflammatory demyelinating disease of the peripheral nervous system, characterized by inflammatory cell infiltration. These inflammatory cells, including activated macrophages, Th1 cells, and Th17 cells, generally undergo metabolic reprogramming and rely mainly on glycolysis to exert functions. This study aimed to explore whether enhanced glycolysis contributed to the pathogenesis of experimental autoimmune neuritis (EAN), a classic model of GBS.
methodsPreventive and therapeutic treatments with glycolysis inhibitor, 2-deoxy-D-glucose (2-DG), were applied to EAN rats. The effects of treatments were determined by clinical scoring, weighting, and tissue examination. Flow cytometry and ELISA were used to evaluate T cell differentiation, autoantibody level, and macrophage functions in vivo and in vitro.
resultsGlycolysis inhibition with 2-DG not only inhibited the initiation, but also prevented the progression of EAN, evidenced by the improved clinical scores, weight loss, inflammatory cell infiltration, and demyelination of sciatic nerves. 2-DG inhibited the differentiation of Th1, Th17, and Tfh cells but enhanced Treg cell development, accompanied with reduced autoantibody secretion. Further experiments in vitro proved glycolysis inhibition decreased the nitric oxide production and phagocytosis of macrophages and suppressed the maturation of dendritic cells (DC).
conclusionThe effects of glycolysis inhibition on both innate and adaptive immune responses and the alleviation of animal clinical symptoms indicated that enhanced glycolysis contributed to the pathogenesis of EAN. Glycolysis inhibition may be a new therapy for GBS.
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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.