Evidence map›Paper›PMID 24058177›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2013

The host environment is responsible for aging-related functional NK cell deficiency.

Bo-Chin Chiu, Brian E Martin, Valerie R Stolberg, Stephen W Chensue

Open access · greenAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

20 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
  2. Immunological biomarkers of aging.Journal of immunology (Baltimore, Md. : 1950) · 2025
    Review
  3. Immune aging and infectious diseases.Chinese medical journal · 2024
    Review
  4. Article
  5. Article
  6. Review
  7. Immune ageing at single-cell resolution.Nature reviews. Immunology · 2022
    Review
  8. Insulin/IGF-1 signaling promotes immunosuppression via the STAT3 pathway: impact on the aging process and age-related diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021
    Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Alcohol, aging, and innate immunity.Journal of leukocyte biology · 2017
    Review
  14. Immune senescence: significance of the stromal microenvironment.Clinical and experimental immunology · 2017
    Review
  15. Review
  16. Article
  17. Review
  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.

Bo-Chin ChiuDepartment of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109.
Brian E Martin
Valerie R Stolberg
Stephen W Chensue
University of Michigan–Ann Arbor · USVA Ann Arbor Healthcare System · US

Funding

CHEMOKINE RECEPTOR DYNAMICS IN GRANULOMA FORMATIONR01AI043460 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CHENSUE, STEPHEN W · 1998 to 2013
$2.3M
NIAID NIH HHS R01 AI043460PHS HHS A143460
6 · The paper itself

Abstract

NK cells play an important role in immunity against infection and tumors. Aging-related functional NK cell deficiency is well documented in humans and mice. However, the mechanism for this is poorly understood. Using an adoptive transfer approach in mice, we found that NK cells from both young and aged mice responded vigorously to priming by pathogen-derived products after being cotransferred into young mice. In contrast, NK cells from young mice responded poorly to priming by pathogen-derived products after being transferred to aged mice. In addition to defects in NK cell priming, maturation of NK cells under steady-state conditions is also impaired in aged mice, resulting in a decreased proportion of CD27(-) mature NK cells. We found that bone marrow from young and aged mice gave rise to CD27(-) mature NK cells similarly in young mixed bone marrow chimeric mice. Furthermore, by using a novel bone marrow transfer approach without irradiation, we found that after being transferred to aged mice, bone marrow from young mice gave rise to NK cells with maturation defects. Finally, we found that aging-related functional NK cell deficiency was completely reversed by injecting soluble IL-15/IL-15Rα complexes. In contrast, blockade of IL-10 signaling, which broadly augments inflammatory responses to pathogen-derived products, had little effect on aging-related defects in NK cell priming. These data demonstrate that the aged host environment is responsible for aging-related functional NK cell deficiency. Additionally, our data suggest that IL-15 receptor agonists may be useful tools in treating aging-related functional NK cell deficiency.

Indexed as

Adoptive TransferAgingAnimalsBone MarrowBone Marrow CellsCell ProliferationCellular SenescenceInterleukin-10Interleukin-15Interleukin-15 Receptor alpha SubunitKiller Cells, NaturalLectins, C-TypeMaleMiceMice, Inbred C57BLReceptors, ImmunologicInterleukin-10Interleukin-15Interleukin-15 Receptor alpha SubunitKlrg1 protein, mouseLectins, C-TypeReceptors, ImmunologicTumor Necrosis Factor Receptor Superfamily, Member 7

Identifiers

PMID24058177
PMCPMC3816106
OpenAlexW2107311712

What OpenQuestion holds

Textmetadata
LicenceTDM
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.