ReviewNature reviews. Immunology2019
At the intersection of DNA damage and immune responses.
Review in Nature reviews. Immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 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
91 citing papers in PubMed, 1 synthesis or guideline pooled it, 151 citations in OpenAlex.
- cGAS in nucleus: The link between immune response and DNA damage repair.Frontiers in immunology · 2022Pooled it
- The Multifunctional SMC5/6 Complex in Genome Stability, Antiviral Restriction, and Human Disease.Current issues in molecular biology · 2026Review
- Mechanistic trends and therapeutic targets in Radiation-Induced apoptosis: A bibliometric and translational mapping.Radiation and environmental biophysics · 2026Review
- Fighting the invader: strategies against intracellular bacteria.Frontiers in pharmacology · 2026Review
- Immune dysfunction in nucleotide excision repair disorders: an underrecognized clinical phenotype with relevance for inborn errors of immunity.Frontiers in immunology · 2026Review
- Integrated peripheral immune profiling reveals B-cell dysregulation and CD8 effector signatures in chronic inflammatory demyelinating polyneuropathy.Frontiers in immunology · 2026Article
- Transcriptional and epigenetic control of human naïve CD8Frontiers in immunology · 2026Article
- Immunosenescence in aging and neurodegenerative diseases: evidence, key hallmarks, and therapeutic implications.Translational neurodegeneration · 2025Review
- DNA double-stranded breaks, a hallmark of aging, defined at the nucleotide resolution, are increased and associated with transcription in the cardiac myocytes in LMNA-cardiomyopathy.Cardiovascular research · 2025Article
- Dynamic crosstalk between amino acid metabolism and cancer drug efficacy: From mechanisms to therapeutic opportunities.iScience · 2025Review
- Immunological Effects of Proton Radiotherapy: New Opportunities and Challenges in Cancer Therapy.Cancer innovation · 2025Review
- Seneca Valley virus infection exploits DNA damage response to facilitate viral replication.Journal of virology · 2025Article
- An mRNA vaccine induces antimycobacterial immunity by activating DNA damage repair and autophagy.Molecular therapy. Nucleic acids · 2025Article
- DDIT3 deficiency ameliorates systemic lupus erythematosus by regulating B cell activation and differentiation.Life medicine · 2025Article
- ATM in immunobiology: From lymphocyte development to cancer immunotherapy.Translational oncology · 2025Review
- Host DNA damage and cellular fate in bacterial infections, with a focus on Staphylococcus aureus.FEMS microbiology reviews · 2025Review
- Characterizing phenotype variants of Cercosporidium personatum, causal agent of peanut late leaf spot disease, their morphology, genetics and metabolites.Scientific reports · 2025Article
- Research progress on the role of the NEIL family in cancer.Frontiers in cell and developmental biology · 2025Review
- Imatinib mesylate reduces c-MYC expression in double-hit lymphoma cells by suppressing inducible cytidine deaminase.Journal of cancer research and clinical oncology · 2024Article
- Article
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
2 authors at 2 institutions in 1 country.
Funding
Abstract
DNA damage occurs on exposure to genotoxic agents and during physiological DNA transactions. DNA double-strand breaks (DSBs) are particularly dangerous lesions that activate DNA damage response (DDR) kinases, leading to initiation of a canonical DDR (cDDR). This response includes activation of cell cycle checkpoints and engagement of pathways that repair the DNA DSBs to maintain genomic integrity. In adaptive immune cells, programmed DNA DSBs are generated at precise genomic locations during the assembly and diversification of lymphocyte antigen receptor genes. In innate immune cells, the production of genotoxic agents, such as reactive nitrogen molecules, in response to pathogens can also cause genomic DNA DSBs. These DSBs in adaptive and innate immune cells activate the cDDR. However, recent studies have demonstrated that they also activate non-canonical DDRs (ncDDRs) that regulate cell type-specific processes that are important for innate and adaptive immune responses. Here, we review these ncDDRs and discuss how they integrate with other signals during immune system development and function.
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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.