ArticleImmunity2025
Oxidative-stress-induced telomere instability drives T cell dysfunction in cancer.
Article in Immunity, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 17 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed.
- Investigating CD8 T Cell Exhaustion in Chronic LCMV Infection by Flow Cytometry.Current protocols · 2026Article
- MUTYH Activity Maintains Telomere Stability in Response to Chronic Telomeric 8-Oxoguanine Damage in Cancer Cells.Biomolecules · 2026Article
- Cellular Senescence and Aging: Mechanisms, Disease Convergence, and Therapeutic Frontiers.MedComm · 2026Review
- SPOCK1 acts as a negative regulator of ferroptosis in non-small cell lung cancer.NPJ precision oncology · 2026Article
- ATG5-mediated inducible autophagy sustains CAR-T cell durability under solid tumor stress.Frontiers in immunology · 2026Article
- Reprogramming CAR T cells across genetic, epigenetic, metabolic and microenvironmental axes to improve efficacy and safety in cancer and autoimmune disease.Frontiers in immunology · 2026Review
- Inhibitory effects of cold atmospheric plasma-activated solution on cutaneous squamous cell carcinoma.Frontiers in pharmacology · 2026Article
- The Five-Decade Journey of Small Cell Lung Cancer.Cancer communications (London, England) · 2026Review
- The Role of Oxidative Stress and Redox Regulation in Cancer.Cancer treatment and research · 2026Review
- Effects of Chronic Intermittent Hypoxia and Subsequent Normoxic Recovery on Renal Senescence and the PI3K/Akt/P21 Pathway in Rats.International journal of nephrology and renovascular disease · 2026Article
- Targeting CAR-T cell exhaustion in non-Hodgkin lymphoma: mechanistic insights and emerging clinical strategies.Frontiers in immunology · 2026Review
- Cancer and Environmental Xenobiotics: Mechanisms, Controversies, and Innovations.Journal of xenobiotics · 2025Review
- Chromosomal Instability and Telomere Attrition in Systemic Sclerosis: A Historical Perspective.Genes · 2025Review
- Genetic approaches for targeted oxidative stress.NAR cancer · 2025Review
- Metabolomic Investigation of Myelodysplastic Syndromes, Multiple Myeloma, and Homozygous β-Thalassemia.Cells · 2025Review
- Brain Region-Specific Epigenomic Reorganization and Altered Cell States in Alzheimer's Disease.bioRxiv : the preprint server for biology · 2025Article
- MDR1 promotes CD8 T cell persistence in tumors and protects against cytotoxic chemotherapy.bioRxiv : the preprint server for biology · 2025Article
Corrections and comments
- Erratum issued
Authors and funding
14 authors.
Funding
Abstract
The tumor microenvironment (TME) imposes immunologic and metabolic stresses sufficient to deviate immune cell differentiation into dysfunctional states. Oxidative stress originating in the mitochondria can induce DNA damage, most notably telomeres. Here, we show that dysfunctional T cells in cancer did not harbor short telomeres indicative of replicative senescence but rather harbored damaged telomeres, which we hypothesized arose from oxidative stress. Chemo-optogenetic induction of highly localized mitochondrial or telomeric reactive oxygen species (ROS) using a photosensitizer caused the accumulation of DNA damage at telomeres, driving telomere fragility. Telomeric damage was sufficient to drive a dysfunctional state in T cells, showing a diminished capability for cytokine production. Localizing the ROS scavenger GPX1 directly to telomeres reduced telomere fragility in tumors and improved the function of therapeutic T cells. Protecting telomeres through expression of a telomere-targeted antioxidant may preserve T cell function in the TME and drive superior responses to cell therapies.
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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.