ArticleCells2019
CD28 Autonomous Signaling Up-Regulates C-Myc Expression and Promotes Glycolysis Enabling Inflammatory T Cell Responses in Multiple Sclerosis.
Article in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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
25 citing papers in PubMed, 40 citations in OpenAlex.
- The Pathogenic Role of T Cell Metabolism and its Effect on Immune Senescence in Autoimmune Diseases and Infection.Clinical reviews in allergy & immunology · 2025Review
- Mapping Molecular Pathways of Multiple Sclerosis: A Gene Prioritization and Network Analysis of White Matter Pathology Transcriptomics.Annals of neurology · 2025Article
- Disease Aggravation With Age in an Experimental Model of Multiple Sclerosis: Role of Immunosenescence.Aging cell · 2025Article
- Influences of metabolism and lipid homeostasis on regulatory vs. conventional T cells and implications for autoimmunity.Frontiers in immunology · 2025Review
- Metabolic regulation of the immune system in health and diseases: mechanisms and interventions.Signal transduction and targeted therapy · 2024Review
- Environmental pollutants and phosphoinositide signaling in autoimmunity.Journal of hazardous materials · 2024Review
- MYC: there is more to it than cancer.Frontiers in cell and developmental biology · 2024Review
- Recovery of intracellular glucose uptake in T cells during partial remission of type 1 diabetes.Diabetologia · 2023Article
- The potential role of T-cell metabolism-related molecules in chronic neuropathic pain after nerve injury: a narrative review.Frontiers in immunology · 2023Review
- Cladribine Reduces Trans-Endothelial Migration of Memory T Cells across an In Vitro Blood-Brain Barrier.Journal of clinical medicine · 2022Article
- Article
- Immune Modulation Using Extracellular Vesicles Encapsulated with MicroRNAs as Novel Drug Delivery Systems.International journal of molecular sciences · 2022Review
- Immune cells transcriptome-based drug repositioning for multiple sclerosis.Frontiers in immunology · 2022Article
- Enhanced T Cell Glucose Uptake Is Associated With Progression of Beta-Cell Function in Type 1 Diabetes.Frontiers in immunology · 2022Article
- The Role of Metabolic Dysfunction in T-Cell Exhaustion During Chronic Viral Infection.Frontiers in immunology · 2022Review
- Comprehensive Assessment of Multiple Sclerosis: From Immunotherapy and Immunopathogenesis to Predictive Biomarkers.Iranian journal of pathology · 2022Review
- Metabolism Characteristics of Th17 and Regulatory T Cells in Autoimmune Diseases.Frontiers in immunology · 2022Review
- Human Wharton's jelly-derived mesenchymal stem cells alleviate concanavalin A-induced fulminant hepatitis by repressing NF-κB signaling and glycolysis.Stem cell research & therapy · 2021Article
- Altered glycolysis results in drug-resistant in clinical tumor therapy.Oncology letters · 2021Review
- A Role for Human Renal Tubular Epithelial Cells in Direct Allo-Recognition by CD4+ T-Cells and the Effect of Ischemia-Reperfusion.International journal of molecular sciences · 2021Article
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 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The immunopathogenesis of multiple sclerosis (MS) depend on the expansion of specific inflammatory T cell subsets, which are key effectors of tissue damage and demyelination. Emerging studies evidence that a reprogramming of T cell metabolism may occur in MS, thus the identification of stimulatory molecules and associated signaling pathways coordinating the metabolic processes that amplify T cell inflammation in MS is pivotal. Here, we characterized the involvement of the cluster of differentiation (CD)28 and associated signaling mediators in the modulation of the metabolic programs regulating pro-inflammatory T cell functions in relapsing-remitting MS (RRMS) patients. We show that CD28 up-regulates glycolysis independent of the T cell receptor (TCR) engagement by promoting the increase of c-myc and the glucose transporter, Glut1, in RRMS CD4
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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.