Evidence map›Paper›PMID 28733462›Full record

ReviewJournal of leukocyte biology2017

Human T cell immunosenescence and inflammation in aging.

Arsun Bektas, Shepherd H Schurman, Ranjan Sen, Luigi Ferrucci

Abstract readReview
In one paragraph

Review in Journal of leukocyte biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 170 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
170citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

170 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Rethinking immune studies: population-level immune variations and the path forward.The journals of gerontology. Series A, Biological sciences and medical sciences · 2026
    Pooled it
  2. Trial
  3. Trial
  4. Article
  5. Article
  6. CD31Physiological reports · 2026
    Article
  7. Review
  8. Review
  9. Review
  10. Tenofovir, Interferon Pathways, and Mucosal Immunity: Implications for People Living With HIV.American journal of reproductive immunology (New York, N.Y. : 1989) · 2026
    Review
  11. Peripheral Immune Remodeling After Spinal Cord Injury: Marked by Expansion of CD38Neurology(R) neuroimmunology & neuroinflammation · 2026
    Observational
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Review
  19. Article
  20. Article

110 more citing papers are in PubMed but not listed here.

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

4 authors.

Arsun BektasTranslational Gerontology Branch, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, USA.
Shepherd H SchurmanClinical Research Branch, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, USA; and.
Ranjan SenLaboratory of Molecular Biology and Immunology, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, USA senra@mail.nih.gov.
Luigi FerrucciTranslational Gerontology Branch, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, USA; ferruccilu@mail.nih.gov.

Funding

Program in Clinical Research, Clinical Support Services and Clinical TrainingZIDES102465 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI KIRSCHNER, LAWRENCE · 2009 to 2025
$84.7M
Age-associated alterations in pro-inflammatory gene expression in humansZIAAG000386 · NIA · NATIONAL INSTITUTE ON AGING · PI SEN, RANJAN · 2009 to 2025
$4.8M
6 · The paper itself

Abstract

The aging process is driven by a finite number of inter-related mechanisms that ultimately lead to the emergence of characteristic phenotypes, including increased susceptibility to multiple chronic diseases, disability, and death. New assays and analytical tools have become available that start to unravel some of these mechanisms. A prevailing view is that aging leads to an imbalance between stressors and stress-buffering mechanisms that causes loss of compensatory reserve and accumulation of unrepaired damage. Central to this paradigm are changes in the immune system and the chronic low-grade proinflammatory state that affect many older individuals, even when they are apparently healthy and free of risk factors. Independent of chronological age, high circulating levels of proinflammatory markers are associated with a high risk of multiple adverse health outcomes in older persons. In this review, we discuss current theories about causes and consequences of the proinflammatory state of aging, with a focus on changes in T cell function. We examine the role of NF-κB activation and its dysregulation and how NF-κB activity differs among subgroups of T cells. We explore emerging hypotheses about immunosenescence and changes in T cell behavior with age, including consideration of the T cell antigen receptor and regulatory T cells (T

Indexed as

AgingAnimalsCellular SenescenceHumansNF-kappa BT-Lymphocytes, RegulatoryNF-kappa Bimmune dysregulationinflamm-agingNF-κB

Identifiers

PMID28733462
PMCPMC5597513

What OpenQuestion holds

Textmetadata
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.