Evidence map›Paper›PMID 26607449›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2015

Temporal fate mapping reveals age-linked heterogeneity in naive T lymphocytes in mice.

Thea Hogan, Graeme Gossel, Andrew J Yates, Benedict Seddon

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

38 citing papers in PubMed, 57 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. The dynamics and longevity of circulating CD4bioRxiv : the preprint server for biology · 2024
    Article
  10. Proteostasis in T cell aging.Seminars in immunology · 2023
    Review
  11. Modeling T Cell Fate.Annual review of immunology · 2023
    Review
  12. Review
  13. Article
  14. Why are cell populations maintained via multiple compartments?Journal of the Royal Society, Interface · 2022
    Article
  15. Article
  16. Review
  17. Article
  18. 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

4 authors at 2 institutions in 1 country.

Thea HoganInstitute of Immunity and Transplantation, Division of Infection and Immunity, University College London, Royal Free Hospital, London NW3 2PF, United Kingdom;
Graeme GosselInstitute of Infection, Immunity & Inflammation, College of Medical, Veterinary & Life Sciences, University of Glasgow, Glasgow G12 8TA, United Kingdom.
Andrew J YatesInstitute of Infection, Immunity & Inflammation, College of Medical, Veterinary & Life Sciences, University of Glasgow, Glasgow G12 8TA, United Kingdom andrew.yates@glasgow.ac.uk benedict.seddon@ucl.ac.uk.
Benedict SeddonInstitute of Immunity and Transplantation, Division of Infection and Immunity, University College London, Royal Free Hospital, London NW3 2PF, United Kingdom; andrew.yates@glasgow.ac.uk benedict.seddon@ucl.ac.uk.
The Royal Free Hospital · GBUniversity of Glasgow · GB

Funding

Modeling the development, structure and regulation of T cell memoryR01AI093870 · NIAID · UNIVERSITY OF GLASGOW · PI YATES, ANDREW · 2011 to 2025
$5.9M
Arthritis Research UKMedical Research Council MC_PC_13055NIAID NIH HHS R01 AI093870NIAID NIH HHS R01AI093870
6 · The paper itself

Abstract

Understanding how our T-cell compartments are maintained requires knowledge of their population dynamics, which are typically quantified over days to weeks using the administration of labels incorporated into the DNA of dividing cells. These studies present snapshots of homeostatic dynamics and have suggested that lymphocyte populations are heterogeneous with respect to rates of division and/or death, although resolving the details of such heterogeneity is problematic. Here we present a method of studying the population dynamics of T cells in mice over timescales of months to years that reveals heterogeneity in rates of division and death with respect to the age of the host at the time of thymic export. We use the transplant conditioning drug busulfan to ablate hematopoetic stem cells in young mice but leave the peripheral lymphocyte compartments intact. Following their reconstitution with congenically labeled (donor) bone marrow, we followed the dilution of peripheral host T cells by donor-derived lymphocytes for a year after treatment. Describing these kinetics with mathematical models, we estimate rates of thymic production, division and death of naive CD4 and CD8 T cells. Population-averaged estimates of mean lifetimes are consistent with earlier studies, but we find the strongest support for a model in which both naive T-cell pools contain kinetically distinct subpopulations of older host-derived cells with self-renewing capacity that are resistant to displacement by naive donor lymphocytes. We speculate that these incumbent cells are conditioned or selected for increased fitness through homeostatic expansion into the lymphopenic neonatal environment.

Indexed as

Cell LineageAgingAnimalsCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesFlow CytometryMaleModels, BiologicalKi67kinetic heterogeneitymathematical modelingT-cell homeostasis

Identifiers

PMID26607449
PMCPMC4687551
OpenAlexW2177466866

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.