Evidence map›Paper›PMID 24145414›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2013

Natural killer cell licensing in mice with inducible expression of MHC class I.

Takashi Ebihara, A Helena Jonsson, Wayne M Yokoyama

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

28 citing papers in PubMed, 43 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Human natural killer cells: Form, function, and development.The Journal of allergy and clinical immunology · 2023
    Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Modulation of NKG2D, NKp46, and Ly49C/I facilitates natural killer cell-mediated control of lung cancer.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  12. Article
  13. [Unlicensed natural killer cells and allogeneic hematopoietic stem cell transplantation].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2017
    Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Cognate HLA absence in trans diminishes human NK cell education.The Journal of clinical investigation · 2016
    Article
  20. Review
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

3 authors at 2 institutions in 1 country.

Takashi EbiharaHoward Hughes Medical Institute and Division of Rheumatology, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110.
A Helena Jonsson
Wayne M Yokoyama
Washington University in St. Louis · USHoward Hughes Medical Institute · US

Funding

INVIVO DEVELOPMENT OF NATURAL KILLER CELLSR01AI033903 · NIAID · WASHINGTON UNIVERSITY · PI YOKOYAMA, WAYNE M. · 1992 to 2015
$4.0M
Howard Hughes Medical InstituteNIAID NIH HHS R01 AI033903NIAID NIH HHS R01-AI033903
6 · The paper itself

Abstract

Mouse natural killer (NK) cells acquire effector function by an education process termed "licensing" mediated by inhibitory Ly49 receptors which recognize self-MHC class I. Ly49 receptors can bind to MHC class I on targets (in trans) and also to MHC class I on the NK-cell surface (in cis). Which of these interactions regulates NK-cell licensing is not yet clear. Moreover, there are no clear phenotypic differences between licensed and unlicensed NK cells, perhaps because of the previously limited ability to study NK cells with synchronized licensing. Here, we produced MHC class I-deficient mice with inducible MHC class I consisting of a single-chain trimer (SCT), ovalbumin peptide-β2 microgloblin-H2K(b) (SCT-K(b)). Only NK cells with a Ly49 receptor with specificity for SCT-K(b) were licensed after MHC class I induction. NK cells were localized consistently in red pulp of the spleen during induced NK-cell licensing, and there were no differences in maturation or activation markers on recently licensed NK cells. Although MHC class I-deficient NK cells were licensed in hosts following SCT-K(b) induction, NK cells were not licensed after induced SCT-K(b) expression on NK cells themselves in MHC class I-deficient hosts. Furthermore, hematopoietic cells with induced SCT-K(b) licensed NK cells more efficiently than stromal cells. These data indicate that trans interaction with MHC class I on hematopoietic cells regulates NK-cell licensing, which is not associated with other obvious phenotypic changes.

Indexed as

Adoptive TransferAnimalsHematopoietic Stem CellsHistocompatibility Antigens Class IImmunohistochemistryKiller Cells, NaturalLymphocyte ActivationMiceMice, Inbred C57BLMice, TransgenicNK Cell Lectin-Like Receptor Subfamily AReceptors, Natural Killer CellSpleenHistocompatibility Antigens Class INK Cell Lectin-Like Receptor Subfamily AReceptors, Natural Killer Cellimmunitylymphocytestolerance

Identifiers

PMID24145414
PMCPMC3831452
OpenAlexW2074769713

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.