Evidence map›Paper›PMID 24873973›Full record

ArticlePLoS pathogens2014

Ly49C-dependent control of MCMV Infection by NK cells is cis-regulated by MHC Class I molecules.

Catherine A Forbes, Anthony A Scalzo, Mariapia A Degli-Esposti, Jerome D Coudert

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

12 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. NK cells in host responses to viral infections.Current opinion in immunology · 2017
    Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
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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.

Catherine A ForbesCentre for Experimental Immunology, Lions Eye Institute, Nedlands, Western Australia, Australia.
Anthony A ScalzoCentre for Experimental Immunology, Lions Eye Institute, Nedlands, Western Australia, Australia.
Mariapia A Degli-EspostiCentre for Experimental Immunology, Lions Eye Institute, Nedlands, Western Australia, Australia; Centre for Ophthalmology and Vision Science, M517, University of Western Australia, Crawley, Western Australia, Australia.
Jerome D CoudertCentre for Experimental Immunology, Lions Eye Institute, Nedlands, Western Australia, Australia; Centre for Ophthalmology and Vision Science, M517, University of Western Australia, Crawley, Western Australia, Australia.
Lions Eye Institute · AUUniversity of Western Australia · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Natural Killer (NK) cells are crucial in early resistance to murine cytomegalovirus (MCMV) infection. In B6 mice, the activating Ly49H receptor recognizes the viral m157 glycoprotein on infected cells. We previously identified a mutant strain (MCMVG1F) whose variant m157 also binds the inhibitory Ly49C receptor. Here we show that simultaneous binding of m157 to the two receptors hampers Ly49H-dependent NK cell activation as Ly49C-mediated inhibition destabilizes NK cell conjugation with their targets and prevents the cytoskeleton reorganization that precedes killing. In B6 mice, as most Ly49H+ NK cells do not co-express Ly49C, the overall NK cell response remains able to control MCMVm157G1F infection. However, in B6 Ly49C transgenic mice where all NK cells express the inhibitory receptor, MCMV infection results in altered NK cell activation associated with increased viral replication. Ly49C-mediated inhibition also regulates Ly49H-independent NK cell activation. Most interestingly, MHC class I regulates Ly49C function through cis-interactions that mask the receptor and restricts m157 binding. B6 Ly49C Tg, β2m ko mice, whose Ly49C receptors are unmasked due to MHC class I deficient expression, are highly susceptible to MCMVm157G1F and are unable to control a low-dose infection. Our study provides novel insights into the mechanisms that regulate NK cell activation during viral infection.

Indexed as

MuromegalovirusAnimalsCytomegalovirus InfectionsHistocompatibility Antigens Class IKiller Cells, NaturalMiceMice, Inbred C57BLMice, TransgenicNK Cell Lectin-Like Receptor Subfamily AHistocompatibility Antigens Class IKlra3 protein, mouseNK Cell Lectin-Like Receptor Subfamily A

Identifiers

PMID24873973
PMCPMC4038614
OpenAlexW1968359003

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.