ArticleScience translational medicine2016
Restoring oxidant signaling suppresses proarthritogenic T cell effector functions in rheumatoid arthritis.
Article in Science translational medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 174 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
174 citing papers in PubMed, 270 citations in OpenAlex.
- Trial
- Dimethyl fumarate treatment restrains the antioxidative capacity of T cells to control autoimmunity.Brain : a journal of neurology · 2021Trial
- Decreased Peripheral Naïve T Cell Number and Its Role in Predicting Cardiovascular and Infection Events in Hemodialysis Patients.Frontiers in immunology · 2021Trial
- Gene expression regulated by abatacept associated with methotrexate and correlation with disease activity in rheumatoid arthritis.PloS one · 2020Trial
- Temperature extremes and autoimmune diseases.Seminars in immunopathology · 2026Review
- Metabolic switch: lymphocytes and the onset of T-cell-mediated autoimmunity.Cellular & molecular immunology · 2026Review
- Lactate Accelerates Early Angiogenesis and Bone Regeneration Through Macrophage M1 Polarisation.Cell proliferation · 2026Article
- Disruption of Treg Homeostasis in Rheumatoid Arthritis via Ferroptosis-Mediated ETC Collapse and TXK-STAT3/PLCγ1 Activation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Gene Expression Alterations in Peripheral Blood Mononuclear Cells and Cartilage Explants from End-Stage Rheumatoid Arthritis Patients in Response to Taurine: A Pilot Exploratory Study.Life (Basel, Switzerland) · 2026Article
- Macrophage metabolic exhaustion and PANoptotic cell death drive chronic tissue inflammation in rheumatoid arthritis.Immunity · 2026Article
- Lipid droplet-induced T cell death sustains autoimmune tissue inflammation.Cell metabolism · 2026Article
- Th17 cells require the DNA repair sensor xeroderma pigmentosum complementation Group C to control oxidative DNA damage in a murine model.Nature communications · 2026Article
- Disturbances in Central Sensitization Are Associated with Disease Severity and Alterations in Gene Expression Measured in the Peripheral Blood Mononuclear Cells of Patients with Rheumatoid Arthritis.International journal of molecular sciences · 2026Article
- Cytotoxic CD4Signal transduction and targeted therapy · 2026Review
- Reductive stress in cancer immunology and targeted therapy.Acta biochimica et biophysica Sinica · 2026Review
- Cyclodextrin Inhibits Caveolin-1 to Regulate CD4Journal of immunology research · 2026Article
- The research progress on the role of glucose-6-phosphate dehydrogenase in immune regulation.PeerJ · 2026Review
- Succinate-mediated metabolic alterations and signaling in RA: mechanisms and therapeutic implications.Frontiers in immunology · 2026Review
- Integrating T cell signaling and metabolism to enhance T cell engager responses in solid tumors.Frontiers in immunology · 2026Review
- GZMK⁺CD8⁺ T Cells Induce Acinar Cell Senescence and Salivary Secretion Impairment in Sjögren's Syndrome via Mitochondrial Dysfunction and TMEM16A Chloride Channel Disruption.International journal of biological sciences · 2026Article
114 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
In patients with rheumatoid arthritis (RA), CD4(+)T cells hyperproliferate during clonal expansion, differentiating into cytokine-producing effector cells that contribute to disease pathology. However, the metabolic underpinnings of this hyperproliferation remain unclear. In contrast to healthy T cells, naïve RA T cells had a defect in glycolytic flux due to the up-regulation of glucose-6-phosphate dehydrogenase (G6PD). Excess G6PD shunted glucose into the pentose phosphate pathway, resulting in NADPH (reduced form of nicotinamide adenine dinucleotide phosphate) accumulation and reactive oxygen species (ROS) consumption. With surplus reductive equivalents, RA T cells insufficiently activated the redox-sensitive kinase ataxia telangiectasia mutated (ATM), bypassed the G2/M cell cycle checkpoint, and hyperproliferated. Moreover, insufficient ATM activation biased T cell differentiation toward the T helper 1 (TH1) and TH17 lineages, imposing a hyperinflammatory phenotype. We have identified several interventions that replenish intracellular ROS, which corrected the abnormal proliferative behavior of RA T cells and successfully suppressed synovial inflammation. Thus, rebalancing glucose utilization and restoring oxidant signaling may provide a therapeutic strategy to prevent autoimmunity in RA.
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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.