ArticleCell death & disease2018
Resting T cells are hypersensitive to DNA damage due to defective DNA repair pathway.
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
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
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
- DNA repair phenotype and cancer risk: a systematic review and meta-analysis of 55 case-control studies.Scientific reports · 2022Pooled it
- Syndecan-4 in microglia mediates ischemic stroke-induced mitochondrial dysfunction and blood-brain barrier damage by interacting with Dishevelled.Scientific reports · 2026Article
- Transient ATR inhibition following ionizing radiation enhances immune-mediated antitumor response and survival.bioRxiv : the preprint server for biology · 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
- Differential Radiosensitivity in T-Cell Subsets: Metabolic and Antioxidative Mechanisms Underlying Naïve T-Cell Vulnerability.Radiation research · 2026Article
- Gene expression changes in lymphocytes and monocytes from patients with traumatic brain injury.Scientific reports · 2026Article
- CLNS1A regulates genome stability and cell cycle progression to control CD4 T cell function and autoimmunity.Science immunology · 2025Article
- Transcriptional signature of rapidly responding NK cells reveals S1P5 and CXCR4 as anti-tumor response disruptors.Scientific reports · 2025Article
- Elucidating the immunomodulatory roles and mechanisms of CUL4B in the immune system: a comprehensive review.Frontiers in immunology · 2025Review
- Modulation of TCR stimulation and pifithrin-α improve the genomic safety profile of CRISPR-engineered human T cells.Cell reports. Medicine · 2024Article
- Expression quantitative trait loci influence DNA damage-induced apoptosis in cancer.BMC genomics · 2024Article
- Transposable elements contribute to tissue-specific gene regulation in humans.Genes & genomics · 2024Article
- Review
- Multiwell-based G0-PCC assay for radiation biodosimetry.Scientific reports · 2024Article
- The multifaceted functions of DNA-PKcs: implications for the therapy of human diseases.MedComm · 2024Review
- Profiling Proteins and Phosphorylation Sites During T Cell Activation Using an Integrated Thermal Shift Assay.Molecular & cellular proteomics : MCP · 2024Article
- Advancing precision cancer immunotherapy drug development, administration, and response prediction with AI-enabled Raman spectroscopy.Frontiers in immunology · 2024Review
- Autoimmunity and immunodeficiency associated with monoallelic LIG4 mutations via haploinsufficiency.The Journal of allergy and clinical immunology · 2023Article
- Ku70 affects the frequency of chromosome translocation in human lymphocytes after radiation and T-cell acute lymphoblastic leukemia.Radiation oncology (London, England) · 2022Article
- CTLA-4 Facilitates DNA Damage-Induced Apoptosis by Interacting With PP2A.Frontiers in cell and developmental biology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Blood cells are challenged by intrinsic and exogenous stress that may result in many types of damage to DNA. As a major participant in cell-mediated immunity in blood, T lymphocytes are maintained in their quiescent (resting) state for most of their lives and switch to the proliferating state once stimulated. How resting and stimulated T cells address DNA damage remains largely unknown. Here, we report that while different types of DNA damage are efficiently repaired in stimulated T cells, they result in massive apoptosis of resting T cells. Mechanistically, DNA damage in resting T cells activates the ATM/ATR/DNA-PKcs signaling pathway but fails to induce the formation of γH
Indexed as
Identifiers
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.