Evidence map›Paper›PMID 28474506›Full record

ArticleImmunity, inflammation and disease2017

Expression of the inhibitory receptor NKG2A correlates with increased liver and splenic NK cell response to activating receptor engagement.

Claire E Meyer, Phillip N Key, Toby Zhu, Mark Shabsovich, Ann Ni, Sandeep K Tripathy

Open access · goldAbstract read
In one paragraph

Article in Immunity, inflammation and disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.4field-weighted citation impact, top 39% 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

4 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. 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

6 authors at 1 institution in 1 country.

Claire E MeyerGastroenterology Division, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri, USA.
Phillip N KeyGastroenterology Division, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri, USA.
Toby ZhuGastroenterology Division, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri, USA.
Mark ShabsovichGastroenterology Division, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri, USA.
Ann NiGastroenterology Division, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri, USA.
Sandeep K TripathyGastroenterology Division, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri, USA.ORCID 0000-0003-1680-7960
Washington University in St. Louis · US

Funding

CLINICAL/LABORATORY TRAINING ACADEMIC GASTROENTEROLOGYT32DK007130 · NIDDK · WASHINGTON UNIVERSITY · PI MATTHEW AARON CIORBA · 1986 to 2026
$8.3M
MECHANISMS OF NATURAL KILLER CELL TOLERANCER01AI089870 · NIAID · WASHINGTON UNIVERSITY · PI TRIPATHY, SANDEEP KUMAR · 2011 to 2014
$1.5M
NIAID NIH HHS R01 AI089870NIDDK NIH HHS T32 DK007130
6 · The paper itself

Abstract

introductionNatural killer (NK) cells play a critical role in the innate immune response to viruses and tumors, and comprise a large proportion of the hepatic lymphocyte population. They must remain tolerant to non-pathogenic antigens while protecting the host from harmful agents. Herein, we investigate how the NK cell response to activation receptor engagement is altered in the liver.

methodsIn this study, we assess IFN-γ production and degranulation of splenic NK cells and selected subsets of liver NK cells. Flow cytometry (FCM) was used to asses IFN-γ production and degranulation following stimulation of the NK cells with plate bound antibodies to activating receptors.

resultsWe show that smaller percentages of hepatic NK cells produce interferon (IFN)-γ and/or degranulate than do splenic NK cells upon stimulation through activating receptors. We also found that smaller percentages of the circulating NK (cNK) cells in the liver produce IFN-γ and/or degranulate, compared to the liver tissue resident NK (trNK) cells. In addition, IFN-γ production by liver cNK cells is not increased in IL-10 deficient mice, suggesting that their hyporesponsiveness is not mediated by the presence of this anti-inflammatory cytokine in the hepatic microenvironment. On the other hand, liver trNK cells express higher levels of the inhibitory receptor NKG2A than do cNK cells, correlating with their increased IFN-γ production and degranulation.

conclusionsLiver cNK cells' hyporesponsiveness to stimulation through activating receptors is independent of IL-10, but correlates with decreased NKG2A expression compared to trNK cells. In addition, we demonstrate that liver NK cells become further hyporesponsive upon continuous engagement of an activating receptor on their cell surface.

Indexed as

AnimalsGene Expression RegulationInterferon-gammaInterleukin-10Killer Cells, NaturalLiverMiceMice, KnockoutNK Cell Lectin-Like Receptor Subfamily COrgan SpecificitySpleenIFNG protein, mouseIL10 protein, mouseInterferon-gammaInterleukin-10NK Cell Lectin-Like Receptor Subfamily CadaptationcytokinesleukocytesmicroenvironmentTolerance

Identifiers

PMID28474506
PMCPMC5418142
OpenAlexW2605404350

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.