Evidence map›Paper›PMID 25612621›Full record

ArticleBlood2015

The mouse NKR-P1B:Clr-b recognition system is a negative regulator of innate immune responses.

Mir Munir A Rahim, Peter Chen, Amelia N Mottashed, Ahmad Bakur Mahmoud, Midhun J Thomas, Qinzhang Zhu, Colin G Brooks, Vicky Kartsogiannis, Matthew T Gillespie, James R Carlyle and 1 more

Open access · bronzeAbstract readComparative Study
PubMed Full text at PMC Publisher
In one paragraph

Article in Blood, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

24 citing papers in PubMed, 42 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Recognition ofInnate immunity · 2023
    Review
  6. Article
  7. Review
  8. Article
  9. Natural killer cells: a promising immunotherapy for cancer.Journal of translational medicine · 2022
    Review
  10. Article
  11. Review
  12. Host genetic control of natural killer cell diversity revealed in the Collaborative Cross.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. 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

11 authors at 7 institutions in 3 countries.

Mir Munir A RahimDepartment of Biochemistry, Microbiology, and Immunology, University of Ottawa, Ottawa, ON, Canada;
Peter ChenDepartment of Immunology, University of Toronto, Sunnybrook Research Institute, Toronto, ON, Canada;
Amelia N MottashedDepartment of Biochemistry, Microbiology, and Immunology, University of Ottawa, Ottawa, ON, Canada;
Ahmad Bakur MahmoudDepartment of Biochemistry, Microbiology, and Immunology, University of Ottawa, Ottawa, ON, Canada; College of Applied Medical Sciences, Taibah University, Madinah Munawwarah, Kingdom of Saudi Arabia;
Midhun J ThomasDepartment of Biochemistry, Microbiology, and Immunology, University of Ottawa, Ottawa, ON, Canada;
Qinzhang ZhuTransgenic Core Facility, Clinical Research Institute of Montreal, Montreal, QC, Canada;
Colin G BrooksInstitute of Cell and Molecular Biosciences, The Medical School, Newcastle, United Kingdom;
Vicky KartsogiannisPrince Henry's Institute, Monash Medical Centre, Clayton, VIC, Australia; and.
Matthew T GillespiePrince Henry's Institute, Monash Medical Centre, Clayton, VIC, Australia; and Department of Biochemistry and Molecular Biology, Monash University, Clayton, VIC, Australia.
James R CarlyleDepartment of Immunology, University of Toronto, Sunnybrook Research Institute, Toronto, ON, Canada;
Andrew P MakrigiannisDepartment of Biochemistry, Microbiology, and Immunology, University of Ottawa, Ottawa, ON, Canada;
University of Ottawa · CAMonash Medical Centre · AUMonash University · AUMontreal Clinical Research Institute · CASunnybrook Health Science Centre · CATaibah University · SAUniversity of Toronto · CA

Funding

Biotechnology and Biological Sciences Research CouncilCanadian Institutes of Health Research 86630
6 · The paper itself

Abstract

NKR-P1B is a homodimeric type II transmembrane C-type lectinlike receptor that inhibits natural killer (NK) cell function upon interaction with its cognate C-type lectin-related ligand, Clr-b. The NKR-P1B:Clr-b interaction represents a major histocompatibility complex class I (MHC-I)-independent missing-self recognition system that monitors cellular Clr-b levels. We have generated NKR-P1B(B6)-deficient (Nkrp1b(-/-)) mice to study the role of NKR-P1B in NK cell development and function in vivo. NK cell inhibition by Clr-b is abolished in Nkrp1b(-/-) mice, confirming the inhibitory nature of NKR-P1B(B6). Inhibitory receptors also promote NK cell tolerance and responsiveness to stimulation; hence, NK cells expressing NKR-P1B(B6) and Ly49C/I display augmented responsiveness to activating signals vs NK cells expressing either or none of the receptors. In addition, Nkrp1b(-/-) mice are defective in rejecting cells lacking Clr-b, supporting a role for NKR-P1B(B6) in MHC-I-independent missing-self recognition of Clr-b in vivo. In contrast, MHC-I-dependent missing-self recognition is preserved in Nkrp1b(-/-) mice. Interestingly, spontaneous myc-induced B lymphoma cells may selectively use NKR-P1B:Clr-b interactions to escape immune surveillance by wild-type, but not Nkrp1b(-/-), NK cells. These data provide direct genetic evidence of a role for NKR-P1B in NK cell tolerance and MHC-I-independent missing-self recognition.

Indexed as

AnimalsBlotting, WesternCells, CulturedFemaleFlow CytometryHistocompatibility Antigens Class IImmunity, InnateKiller Cells, NaturalLectins, C-TypeLigandsLymphoma, B-CellMaleMembrane ProteinsMiceMice, Inbred C57BLNK Cell Lectin-Like Receptor Subfamily BHistocompatibility Antigens Class IKlrb1b protein, mouseLectins, C-TypeLigandsMembrane ProteinsNK Cell Lectin-Like Receptor Subfamily BOcil protein, mouse

Identifiers

PMID25612621
PMCPMC4383798
OpenAlexW1991469355

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.