Evidence map›Paper›PMID 18606857›Full record

ArticleThe Journal of experimental medicine2008

Continuous engagement of a self-specific activation receptor induces NK cell tolerance.

Sandeep K Tripathy, Peter A Keyel, Liping Yang, Jeanette T Pingel, Tammy P Cheng, Achim Schneeberger, Wayne M Yokoyama

Abstract read
In one paragraph

Article in The Journal of experimental medicine, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers.

0numbers the graph read from it
0cells of the map it votes in
93citing papers in PubMed
–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

93 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. An inference model gives insights into innate immune adaptation and repertoire diversity.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. NK Cells and ILC1s in Cancer Biology.Advances in experimental medicine and biology · 2022
    Review
  11. Review
  12. Review
  13. Polyvalent design in the cGAS-STING pathway.Seminars in immunology · 2021
    Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Review
  20. Article

33 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

7 authors.

Sandeep K TripathyGastroenterology Division, Department of Medicine, Washington University School of Medicine and Howard Hughes Medical Institute, St. Louis, MO 63110, USA.
Peter A Keyel
Liping Yang
Jeanette T Pingel
Tammy P Cheng
Achim Schneeberger
Wayne M Yokoyama

Funding

Washington University DDRCC Supplemental Equipment RequestP30DK052574 · NIDDK · WASHINGTON UNIVERSITY · PI Nicholas O. Davidson · 2000 to 2026
$30.8M
Viral Discovery in Rheumatoid ArthritisP30AR048335 · NIAMS · WASHINGTON UNIVERSITY · PI WEIHL, CONRAD C · 2001 to 2015
$8.9M
Howard Hughes Medical InstituteNIAMS NIH HHS P30 AR048335NIAMS NIH HHS P30-AR48335NIDDK NIH HHS 5P30 DK052574NIDDK NIH HHS P30 DK052574PHS HHS K08 A1071016-01
6 · The paper itself

Abstract

Natural killer (NK) cell tolerance mechanisms are incompletely understood. One possibility is that they possess self-specific activation receptors that result in hyporesponsiveness unless modulated by self-major histocompatability complex (MHC)-specific inhibitory receptors. As putative self-specific activation receptors have not been well characterized, we studied a transgenic C57BL/6 mouse that ubiquitously expresses m157 (m157-Tg), which is the murine cytomegalovirus (MCMV)-encoded ligand for the Ly49H NK cell activation receptor. The transgenic mice were more susceptible to MCMV infection and were unable to reject m157-Tg bone marrow, suggesting defects in Ly49H(+) NK cells. There was a reversible hyporesponsiveness of Ly49H(+) NK cells that extended to Ly49H-independent stimuli. Continuous Ly49H-m157 interaction was necessary for the functional defects. Interestingly, functional defects occurred when mature wild-type NK cells were adoptively transferred to m157-Tg mice, suggesting that mature NK cells may acquire hyporesponsiveness. Importantly, NK cell tolerance caused by Ly49H-m157 interaction was similar in NK cells regardless of expression of Ly49C, an inhibitory receptor specific for a self-MHC allele in C57BL/6 mice. Thus, engagement of self-specific activation receptors in vivo induces an NK cell tolerance effect that is not affected by self-MHC-specific inhibitory receptors.

Indexed as

Immune ToleranceAdoptive TransferAnimalsAntigens, LyBone Marrow TransplantationCell DifferentiationHerpesviridae InfectionsKiller Cells, Lymphokine-ActivatedKiller Cells, NaturalLectins, C-TypeLigandsLymphocyte ActivationMembrane GlycoproteinsMiceMice, Inbred C57BLMice, TransgenicAntigens, LyKlra3 protein, mouseKlra8 protein, mouseLectins, C-TypeLigandsMembrane GlycoproteinsNK Cell Lectin-Like Receptor Subfamily AReceptors, ImmunologicReceptors, NK Cell Lectin-LikeViral Proteins

Identifiers

PMID18606857
PMCPMC2525593

What OpenQuestion holds

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Registered trials

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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.