ArticleScience signaling2017
Aging impairs both primary and secondary RIG-I signaling for interferon induction in human monocytes.
Article in Science signaling, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers, 2 of them syntheses that pooled it.
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
106 citing papers in PubMed, 2 syntheses or guidelines pooled it, 155 citations in OpenAlex.
- Circulating Type I Interferon Levels and COVID-19 Severity: A Systematic Review and Meta-Analysis.Frontiers in immunology · 2021Pooled it
- Severe COVID-19: what have we learned with the immunopathogenesis?Advances in rheumatology (London, England) · 2020Pooled it
- Remodeling of innate antiviral immunity in aging.Cell insight · 2026Review
- Cellular Senescence Dysregulates Antiviral Interferon Responses in Idiopathic Pulmonary Fibrosis.Aging cell · 2026Article
- Immunosenescence and cancer predisposition in pediatric transplant recipients: An emerging paradigm.World journal of transplantation · 2026Review
- Article
- Striking the right balance with type I interferon signalling in cancer.Nature reviews. Cancer · 2026Review
- Cellular senescence dysregulates antiviral interferon responses in idiopathic pulmonary fibrosis.bioRxiv : the preprint server for biology · 2026Article
- Integrated drivers of basal and acute immunity in diverse human populations.Cell reports. Medicine · 2026Article
- Antiviral CD4Communications medicine · 2026Article
- Senescent Factors Suppress Innate Antiviral Immunity in Aged Mice via Two Distinct Mechanisms.Aging cell · 2026Article
- Age-Associated Inflammatory Monocytes Are Increased in Menopausal Females and Reversed by Hormone Replacement Therapy.Aging cell · 2025Article
- High seroprevalence and high risk: why are older adults more prone to respiratory syncytial virus?Journal of virology · 2025Review
- Intranasal hemagglutinin protein boosters induce protective mucosal immunity against influenza A viruses in mice.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- ApoD mediates age-associated increase in vulnerability to influenza virus infection.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Reduction of TRAF3 by heterozygosity or aging impacts B cell function.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Elderly individuals exhibit dysregulated monocyte responses to viral immune complexes compared to adults and children.Scientific reports · 2025Article
- Increased IFN responses drive myeloid cell activation in people living with HIV-1.Scientific reports · 2025Article
- Aging-associated changes in immunological parameters: Implications for COVID-19 immune response in the elderly.Physiological reports · 2025Review
- Article
46 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
6 authors at 3 institutions in 1 country.
Funding
Abstract
Adults older than 65 account for most of the deaths caused by respiratory influenza A virus (IAV) infections, but the underlying mechanisms for this susceptibility are poorly understood. IAV RNA is detected by the cytosolic sensor retinoic acid-inducible gene I (RIG-I), which induces the production of type I interferons (IFNs) that curtail the spread of the virus and promote the elimination of infected cells. We have previously identified a marked defect in the IAV-inducible secretion of type I IFNs, but not proinflammatory cytokines, in monocytes from older (>65 years) healthy human donors. We found that monocytes from older adults exhibited decreased abundance of the adaptor protein TRAF3 (tumor necrosis factor receptor-associated factor 3) because of its increased proteasomal degradation with age, thereby impairing the primary RIG-I signaling pathway for the induction of type I IFNs. We determined that monocytes from older adults also failed to effectively stimulate the production of the IFN regulatory transcription factor IRF8, which compromised IFN induction through secondary RIG-I signaling. IRF8 played a central role in IFN induction in monocytes, because knocking down IRF8 in monocytes from younger adults was sufficient to replicate the IFN defects observed in monocytes from older adults, whereas restoring IRF8 expression in older adult monocytes was sufficient to restore RIG-I-induced IFN responses. Aging thus compromises both the primary and secondary RIG-I signaling pathways that govern expression of type I IFN genes, thereby impairing antiviral resistance to IAV.
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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.