ArticleJournal of immunology (Baltimore, Md. : 1950)2015
Age-Associated Failure To Adjust Type I IFN Receptor Signaling Thresholds after T Cell Activation.
Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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
39 citing papers in PubMed, 55 citations in OpenAlex.
- Not all reference samples are equal in single-cell transcriptomics of human kidney tissue.JCI insight · 2026Article
- Antiviral CD4Communications medicine · 2026Article
- Cell-Intrinsic Type I Interferon Signaling as a Pleiotropic Orchestrator of CD4 T Cell Immunity.Biomolecules · 2026Review
- Auto-Abs against type I IFNs: Strong, common, and global determinants of severe arboviral diseases.Journal of human immunity · 2026Review
- Rewired type I IFN signaling is linked to age-dependent differences in COVID-19.Cell reports. Medicine · 2025Article
- Th1-poised naive CD4 T cell subpopulation reflects anti-tumor immunity and autoimmune disease.Nature communications · 2025Article
- Chronic inflammation degrades CD4 T cell immunity to prior vaccines in treated HIV infection.Nature communications · 2024Article
- TIGIT reverses IFN-α-promoted Th1-like Tregs via in-sequence effects dependent on STAT4.Arthritis research & therapy · 2023Article
- Counteracting Immunosenescence-Which Therapeutic Strategies Are Promising?Biomolecules · 2023Review
- How much (evil) intelligence can be encoded by 30 kb?Biologia futura · 2023Article
- Human Listeriosis.Clinical microbiology reviews · 2023Review
- COVID-19 diverse outcomes: Aggravated reinfection, type I interferons and antibodies.Medical hypotheses · 2022Article
- Immunosenescence and Altered Vaccine Efficiency in Older Subjects: A Myth Difficult to Change.Vaccines · 2022Review
- Immunology of SARS-CoV-2 infection in children.Nature immunology · 2022Review
- The Th1/Tfh-like biased responses elicited by the rASP-1 innate adjuvant are dependent on TRIF and Type I IFN receptor pathways.Frontiers in immunology · 2022Article
- Molecular Function of cGAS-STING in SARS-CoV-2: A Novel Approach to COVID-19 Treatment.BioMed research international · 2022Review
- Hallmarks of the aging T-cell system.The FEBS journal · 2021Review
- Baseline pro-inflammatory gene expression in whole blood is related to adverse long-term outcomes after transcatheter aortic valve replacement: a case control study.BMC cardiovascular disorders · 2021Article
- Review
- COVID-19 in patients with systemic lupus erythematosus: lessons learned from the inflammatory disease.Translational research : the journal of laboratory and clinical medicine · 2021Review
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 at 1 institution in 1 country.
Funding
Abstract
With increasing age, naive CD4 T cells acquire intrinsic defects that compromise their ability to respond and differentiate. Type I IFNs, pervasive constituents of the environment in which adaptive immune responses occur, are known to regulate T cell differentiation and survival. Activated naive CD4 T cells from older individuals have reduced responses to type I IFN, a defect that develops during activation and that is not observed in quiescent naive CD4 T cells. Naive CD4 T cells from young adults upregulate the expression of STAT1 and STAT5 after activation, lowering their threshold to respond to type I IFN stimulation. The heightened STAT signaling is critical to maintain the expression of CD69 that regulates lymphocyte egress and the ability to produce IL-2 and to survive. Although activation of T cells from older adults also induces transcription of STAT1 and STAT5, failure to exclude SHP-1 from the signaling complex blunts their type I IFN response. In summary, our data show that type I IFN signaling thresholds in naive CD4 T cells after activation are dynamically regulated to respond to environmental cues for clonal expansion and memory cell differentiation. Naive CD4 T cells from older adults have a defect in this threshold calibration. Restoring their ability to respond to type I IFN emerges as a promising target to restore T cell responses and to improve the induction of T cell memory.
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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.