Evidence map›Paper›PMID 25553802›Full record

ArticleAging2014

Age-associated changes in basal NF-κB function in human CD4+ T lymphocytes via dysregulation of PI3 kinase.

Arsun Bektas, Yongqing Zhang, Elin Lehmann, William H Wood, Kevin G Becker, Karen Madara, Luigi Ferrucci, Ranjan Sen

Open access · hybridAbstract readComparative Study
In one paragraph

Article in Aging, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.4field-weighted citation impact, top 11% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

36 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
  2. Article
  3. Immune aging and infectious diseases.Chinese medical journal · 2024
    Review
  4. Article
  5. Article
  6. Proteostasis in T cell aging.Seminars in immunology · 2023
    Review
  7. Article
  8. Heterogeneity of memory T cells in aging.Frontiers in immunology · 2023
    Review
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Inflammaging: Age and Systemic, Cellular, and Nuclear Inflammatory Biology in Older Adults.The journals of gerontology. Series A, Biological sciences and medical sciences · 2019
    Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Arsun BektasTranslational Gerontology Branch, National Institute on Aging, Baltimore, MD 21224, USA.
Yongqing ZhangLaboratory of Genetics, National Institute on Aging, Baltimore, MD 21224, USA.
Elin LehmannLaboratory of Genetics, National Institute on Aging, Baltimore, MD 21224, USA.
William H WoodLaboratory of Genetics, National Institute on Aging, Baltimore, MD 21224, USA.
Kevin G BeckerLaboratory of Genetics, National Institute on Aging, Baltimore, MD 21224, USA.
Karen MadaraClinical Research Branch, National Institute on Aging, Baltimore, MD 21224, USA.
Luigi FerrucciTranslational Gerontology Branch, National Institute on Aging, Baltimore, MD 21224, USA.
Ranjan SenLaboratory of Molecular Biology and Immunology, National Institute on Aging, Baltimore, MD 21224, USA.
National Institute on Aging · US

Funding

Analysis of complex biological systems by microarray based gene expressionZICAG000616 · NIA · NATIONAL INSTITUTE ON AGING · PI DE, SUPRIYO · 2009 to 2025
$15.5M
Age-associated alterations in pro-inflammatory gene expression in humansZIAAG000386 · NIA · NATIONAL INSTITUTE ON AGING · PI SEN, RANJAN · 2009 to 2025
$4.8M
Intramural NIH HHS
6 · The paper itself

Abstract

Immune impairment and high circulating level of pro-inflammatory cytokines are landmarks of human aging. However, the molecular basis of immune dys-regulation and the source of inflammatory markers remain unclear. Here we demonstrate that in the absence of overt cell stimulation gene expression mediated by the transcription factor NF-κB is higher in purified and rested human CD4+ T lymphocytes from older compared to younger individuals. This increase of NF-κB -associated transcription includes transcripts for pro-inflammatory cytokines such as IL-1 and chemokines such as CCL2 and CXCL10. We demonstrate that NF-κB up-regulation is cell-intrinsic and mediated in part by phosphatidylinositol 3-kinase (PI3K) activity induced in response to metabolic activity, which can be moderated by rapamycin treatment. Our observations provide direct evidence that dys-regulated basal NF-κB activity may contribute to the mild pro-inflammatory state of aging.

Indexed as

AdultAgedAged, 80 and overAge FactorsAgingCD4-Positive T-LymphocytesCells, CulturedCytokinesFemaleHumansInflammation MediatorsMaleMiddle AgedNF-kappa BPhosphatidylinositol 3-KinasePhosphoinositide-3 Kinase InhibitorsCytokinesInflammation MediatorsNF-kappa BPhosphatidylinositol 3-KinasePhosphoinositide-3 Kinase InhibitorsProtein Kinase InhibitorsSirolimus

Identifiers

PMID25553802
PMCPMC4276789
OpenAlexW91255988

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.