ReviewFrontiers in immunology2018
DNA Damage Response Signals Transduce Stress From Rheumatoid Arthritis Risk Factors Into T Cell Dysfunction.
Review in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 28 citations in OpenAlex.
- Sensing of DNA double-strand breaks by the NHEJ system stabilizes RORγt transcriptional activity and shapes Th17 pathogenicity in autoimmunity.Cell research · 2026Article
- Interpretable neural network for risk stratification and drug target discovery based on PBMC transcriptomes.iScience · 2026Article
- Genotoxic stressors mimicking synovial microenvironment modulate B cell fate in RA-FLS co-culture.Frontiers in immunology · 2026Article
- Association of DNA damage response pathway genes with rheumatoid arthritis risks: a case-control study.Scientific reports · 2025Article
- Functional dissection of noncoding variants associated with rheumatoid arthritis.Annals of the rheumatic diseases · 2025Article
- Transcriptomic insights into the mechanism of action of telomere-related biomarkers in rheumatoid arthritis.Frontiers in immunology · 2025Article
- Identification of Disulfidptosis-Related Genes and Molecular Subgroups in Rheumatoid Arthritis for Diagnostic Model and Patient Stratification.Journal of inflammation research · 2025Article
- Comprehensive and advanced T cell cluster analysis for discriminating seropositive and seronegative rheumatoid arthritis.Frontiers in immunology · 2025Article
- Bivalent chromatin accommodates survivin and BRG1/SWI complex to activate DNA damage response in CD4Cell communication and signaling : CCS · 2024Article
- Nature of the Association between Rheumatoid Arthritis and Cervical Cancer and Its Potential Therapeutic Implications.Nutrients · 2024Review
- The Association between Inefficient Repair of DNA Double-Strand Breaks and Common Polymorphisms of the HRR and NHEJ Repair Genes in Patients with Rheumatoid Arthritis.International journal of molecular sciences · 2024Article
- Article
- Article
- Leucocyte Abnormalities in Synovial Fluid of Degenerative and Inflammatory Arthropathies.International journal of molecular sciences · 2023Article
- Assessing the association of leukocyte telomere length with ankylosing spondylitis and rheumatoid arthritis: A bidirectional Mendelian randomization study.Frontiers in immunology · 2023Article
- Immunosenescence of T cells: a key player in rheumatoid arthritis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Review
- Construction of a Novel LncRNA Signature Related to Genomic Instability to Predict the Prognosis and Immune Activity of Patients With Hepatocellular Carcinoma.Frontiers in immunology · 2022Article
- Decreased ATM Function Causes Delayed DNA Repair and Apoptosis in Common Variable Immunodeficiency Disorders.Journal of clinical immunology · 2021Article
- DNA Damage Response in the Adaptive Arm of the Immune System: Implications for Autoimmunity.International journal of molecular sciences · 2021Review
- Impact of Different JAK Inhibitors and Methotrexate on Lymphocyte Proliferation and DNA Damage.Journal of clinical medicine · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rheumatoid arthritis (RA) is an autoimmune-mediated disease that is associated with significant cartilage damage and immunosenescence. Despite decades of research, the major signal pathways that initiate RA are still unclear. The DNA damage response (DDR) is a specific and hierarchical network that includes cell cycle checkpoints, DNA repair, and DNA-damage tolerance pathways. Recent studies suggest that this condition is associated with deficits in telomere maintenance and overall genomic instability in the T cells of RA patients. Analysis of the underlying mechanisms has revealed defects in DDR pathways. Particularly, the DNA repair enzyme, ataxia telangiectasia mutated (ATM), is downregulated, which leaves the damaged DNA breaks in RA-associated T cells unrepaired and pushes them to apoptosis, exhausts the T cell pool, and promotes the arthritogenesis effector function of T cells. This review discusses recent advancements and illustrates that risk factors for RA, such as viral infections, environmental events, and genetic risk loci are combat with DDR signals, and the impaired DDR response of RA-associated T cells, in turn, triggers disease-related phenotypes. Therefore, DDR is the dominant signal that converts genetic and environmental stress to RA-related immune dysfunction. Understanding the orchestration of RA pathogenesis by DDR signals would further our current knowledge of RA and provide novel avenues in RA therapy.
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.