ReviewNature reviews. Rheumatology2009
Rejuvenating the immune system in rheumatoid arthritis.
Review in Nature reviews. Rheumatology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 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
66 citing papers in PubMed.
- A phase II multicenter rabbit anti-thymocyte globulin trial in patients with myelodysplastic syndromes identifying a novel model for response prediction.Haematologica · 2014Trial
- A natural product telomerase activator as part of a health maintenance program.Rejuvenation research · 2011Trial
- T-Cell Immunosenescence in Systemic Lupus Erythematosus: Molecular Mechanisms and Therapeutic Perspectives.Clinical reviews in allergy & immunology · 2026Review
- The functional roles and mechanisms of polyamines in age-related bone diseases.Cellular and molecular life sciences : CMLS · 2025Review
- Function of p53 in angiogenesis and oxidative stress in rheumatoid arthritis.Clinical and experimental medicine · 2025Review
- Iron and energy metabolic interactions in Treg-mediated immune regulation.Frontiers in immunology · 2025Review
- Endogenous antigens shape the transcriptome and TCR repertoire in an autoimmune arthritis model.The Journal of clinical investigation · 2024Article
- Research progress of T cell autophagy in autoimmune diseases.Frontiers in immunology · 2024Review
- Small heterodimer partner interacting leucine zipper protein (SMILE) ameliorates autoimmune arthritis via AMPK signaling pathway and the regulation of B cell activation.Cell communication and signaling : CCS · 2023Article
- Mitochondria as disease-relevant organelles in rheumatoid arthritis.Clinical and experimental immunology · 2023Article
- Cellular rejuvenation: molecular mechanisms and potential therapeutic interventions for diseases.Signal transduction and targeted therapy · 2023Review
- The Involvement of Glucose and Lipid Metabolism Alteration in Rheumatoid Arthritis and Its Clinical Implication.Journal of inflammation research · 2023Review
- New Insights into the Pathogenesis of Giant Cell Arteritis: Mechanisms Involved in Maintaining Vascular Inflammation.Journal of clinical medicine · 2022Review
- ZAP70, too little, too much can lead to autoimmunity.Immunological reviews · 2022Review
- Immune cells in cardiac homeostasis and disease: emerging insights from novel technologies.European heart journal · 2022Review
- Frailty as a novel predictor of achieving comprehensive disease control (CDC) in rheumatoid arthritis.Clinical rheumatology · 2021Article
- Metabolomics in Autoimmune Diseases: Focus on Rheumatoid Arthritis, Systemic Lupus Erythematous, and Multiple Sclerosis.Metabolites · 2021Review
- Mortality of Sepsis in Patients With Rheumatoid Arthritis: A Single-Center Retrospective Analysis and Comparison With a Control Group.Journal of intensive care medicine · 2021Article
- Nanomedicines for the treatment of rheumatoid arthritis: State of art and potential therapeutic strategies.Acta pharmaceutica Sinica. B · 2021Review
- Article
6 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
4 authors.
Funding
Abstract
In rheumatoid arthritis (RA), the aging process of the immune system is accelerated. Formerly, this phenomenon was suspected to be a consequence of chronic inflammatory activity. However, newer data strongly suggest that deficiencies in maintaining telomeres and overall DNA stability cause excessive apoptosis of RA T cells, imposing proliferative pressure and premature aging on the system. Already during the early stages of their life cycle, and long before they participate in the inflammatory process, RA T cells are lost owing to increased apoptotic susceptibility. A search for underlying mechanisms has led to the discovery of defective pathways of repairing broken DNA and elongating and protecting telomeric sequences at the chromosomal ends. Two enzymatic machineries devoted to DNA repair and maintenance have been implicated. RA T cells fail to induce sufficient amounts of the telomeric repair enzyme telomerase, leaving telomeric ends uncapped and thus susceptible to damage. Of equal importance, RA T cells produce low levels of the DNA repair enzyme ataxia telangiectasia mutated and the complex of nucleoproteins that sense and fix DNA double-strand breaks. The inability to repair damaged DNA renders naive T cells vulnerable to apoptosis, exhausts T-cell regeneration and reshapes the T cell repertoire. Therapeutic attempts to reset the immune systems of patients with RA and prevent premature immunosenescence should include restoration of DNA repair capability.
Indexed as
Identifiers
19798035What 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.