ReviewArthritis research & therapy2015
T-cell metabolism in autoimmune disease.
Review in Arthritis research & therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
91 citing papers in PubMed, 155 citations in OpenAlex.
- Metabolic switch: lymphocytes and the onset of T-cell-mediated autoimmunity.Cellular & molecular immunology · 2026Review
- Dynamic Metabolic Profiling and Diagnostic Biomarkers of Acute Graft-Versus-Host Disease Based on Metabolomics.Biomedical chromatography : BMC · 2026Article
- A new type of biomarker for heat stress: insights from immunology.Frontiers in immunology · 2026Review
- Dysbiosis of intestinal microbiota in patients with neuromyelitis optica spectrum disorders.Frontiers in immunology · 2026Article
- Identification and Immune Landscape Analysis of Fatty Acid Metabolism-related Genes Associated with Rheumatoid Arthritis.International journal of medical sciences · 2026Article
- Plasma Exosomal LncRNA XIST Impairs CD4Journal of inflammation research · 2026Article
- Piezo1-mediated mechano-energetics regulate CAR T cell function.Research square · 2025Article
- Salidroside: A Potential Drug Candidate to Treat Rheumatoid Arthritis.Molecules (Basel, Switzerland) · 2025Review
- Function ofEJNMMI reports · 2025Article
- Unveiling the Therapeutic Potential: Targeting Fibroblast-like Synoviocytes in Rheumatoid Arthritis.Expert reviews in molecular medicine · 2025Review
- SIRT3 deficiency reduces PFKFB3-driven T-cell glycolysis and promotes arthritic inflammation.Science China. Life sciences · 2025Article
- Intricating connections: the role of ferroptosis in systemic lupus erythematosus.Frontiers in immunology · 2025Review
- Experimental and computational investigation of the kinetic evolution of the glutaminolysis pathway and its interplay with the glycolysis pathway.FEBS open bio · 2024Article
- A global view of T cell metabolism in systemic lupus erythematosus.Frontiers in immunology · 2024Review
- Lower Frequency of Comorbidities Prior to Onset of Giant Cell Arteritis: A Population-Based Study.The Journal of rheumatology · 2023Article
- New sights of immunometabolism and agent progress in colitis associated colorectal cancer.Frontiers in pharmacology · 2023Review
- NAMPT/SIRT1 Expression Levels in White Blood Cells Differentiate the Different Rheumatoid Arthritis Subsets: An Inspiration from Traditional Chinese Medicine.Journal of inflammation research · 2023Article
- Metabolites: fuelling the immune response.Clinical and experimental immunology · 2022Article
- Lupus Susceptibility Loci Predispose Mice to Clonal Lymphocytic Responses and Myeloid Expansion.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Regulation of activated T cell survival in rheumatic autoimmune diseases.Nature reviews. Rheumatology · 2022Review
31 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
4 authors at 3 institutions in 1 country.
Funding
Abstract
Cancer cells have long been known to fuel their pathogenic growth habits by sustaining a high glycolytic flux, first described almost 90 years ago as the so-called Warburg effect. Immune cells utilize a similar strategy to generate the energy carriers and metabolic intermediates they need to produce biomass and inflammatory mediators. Resting lymphocytes generate energy through oxidative phosphorylation and breakdown of fatty acids, and upon activation rapidly switch to aerobic glycolysis and low tricarboxylic acid flux. T cells in patients with rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) have a disease-specific metabolic signature that may explain, at least in part, why they are dysfunctional. RA T cells are characterized by low adenosine triphosphate and lactate levels and increased availability of the cellular reductant NADPH. This anti-Warburg effect results from insufficient activity of the glycolytic enzyme phosphofructokinase and differentiates the metabolic status in RA T cells from those in cancer cells. Excess production of reactive oxygen species and a defect in lipid metabolism characterizes metabolic conditions in SLE T cells. Owing to increased production of the glycosphingolipids lactosylceramide, globotriaosylceramide and monosialotetrahexosylganglioside, SLE T cells change membrane raft formation and fail to phosphorylate pERK, yet hyperproliferate. Borrowing from cancer metabolomics, the metabolic modifications occurring in autoimmune disease are probably heterogeneous and context dependent. Variations of glucose, amino acid and lipid metabolism in different disease states may provide opportunities to develop biomarkers and exploit metabolic pathways as therapeutic targets.
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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.