Evidence map›Paper›PMID 32219494›Full record

ReviewImmunogenetics2020

Tuning of human NK cells by endogenous HLA-C expression.

Frederick J Goodson-Gregg, Stacey A Krepel, Stephen K Anderson

Open access · hybridAbstract readReview
In one paragraph

Review in Immunogenetics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

17 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. Association betweenHeliyon · 2024
    Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. HLA Alleles BFrontiers in immunology · 2021
    Article
  14. Article
  15. Review
  16. Review
  17. Single Nucleotide Polymorphism inFrontiers in immunology · 2020
    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

3 authors at 2 institutions in 1 country.

Frederick J Goodson-GreggLaboratory of Cancer Immunometabolism, Center for Cancer Research, National Cancer Institute, Frederick, MD, 21702, USA.
Stacey A KrepelLaboratory of Cancer Immunometabolism, Center for Cancer Research, National Cancer Institute, Frederick, MD, 21702, USA.
Stephen K AndersonBasic Science Program, Frederick National Laboratory for Cancer Research, Frederick, MD, 21702, USA. andersonst@mail.nih.gov.ORCID 0000-0002-7856-4266
National Cancer Institute · USFrederick National Laboratory for Cancer Research · US

Funding

Molecular Studies of Cellular CytotoxicityZIABC010013 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI ANDERSON, STEPHEN K · 2009 to 2025
$17.2M
NCI NIH HHS HHSN261200800001E
6 · The paper itself

Abstract

NK cells are primarily responsible for detecting malignant or pathogen-infected cells, and their function is influenced both by stress-associated activating signals and opposing inhibitory signals from receptors that recognize self MHC. The receptors that produce this inhibitory signal shift from the NKG2A:HLA-E system to that of KIR:HLA as the NK cells mature. This maturation is associated with an increase in lytic activity, as well as an increase in HLA-C protein levels controlled by the NK-specific HLA-C promoter, NK-Pro. We propose that modulation of the translatability of HLA-C transcripts in NK cells constitutes an evolutionary mechanism to control cis inhibitory signaling by HLA-C, which fine tunes NK cell activity. Furthermore, the high degree of variability in KIR receptor affinity for HLA alleles, as well as the variable expression levels of both KIR and HLA, suggest an evolutionary requirement for the tuning of NK lytic activity. Various data have demonstrated that mature NK cells may gain or lose lytic activity when placed in different environments. This indicates that NK cell activity may be more a function of constant tuning by inhibitory signals, rather than a static, irreversible "license to kill" granted to mature NK cells. Inhibitory signaling controls the filling of the cytolytic granule reservoir, which becomes depleted if there are insufficient inhibitory signals, leading to a hyporesponsive NK cell. We propose a novel model for the tuning of human NK cell activity via cis interactions in the context of recent findings on the mechanism of NK education.

Indexed as

AllelesAnimalsHLA-C AntigensHumansKiller Cells, NaturalMiceOrgan SpecificityReceptors, KIR2DL1HLA-C AntigensKIR2DL1 protein, humanReceptors, KIR2DL1ArmingHLA-CLicensingNKNK educationNK promoter

Identifiers

PMID32219494
PMCPMC7182622
OpenAlexW3013750740

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.