Evidence map›Paper›PMID 30696399›Full record

ArticleBMC immunology2019

Expression of ligands for activating natural killer cell receptors on cell lines commonly used to assess natural killer cell function.

Alexandra Tremblay-McLean, Sita Coenraads, Zahra Kiani, Franck P Dupuy, Nicole F Bernard

Open access · goldAbstract read
In one paragraph

Article in BMC immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

39 citing papers in PubMed, 52 citations in OpenAlex.

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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

5 authors at 1 institution in 1 country.

Alexandra Tremblay-McLeanResearch Institute of the McGill University Health Center, Glen Site, 1001 Décarie Boulevard, Block E, Rm EM3.3238, Montréal, Québec, H4A 3J1, Canada.
Sita CoenraadsResearch Institute of the McGill University Health Center, Glen Site, 1001 Décarie Boulevard, Block E, Rm EM3.3238, Montréal, Québec, H4A 3J1, Canada.
Zahra KianiResearch Institute of the McGill University Health Center, Glen Site, 1001 Décarie Boulevard, Block E, Rm EM3.3238, Montréal, Québec, H4A 3J1, Canada.
Franck P DupuyResearch Institute of the McGill University Health Center, Glen Site, 1001 Décarie Boulevard, Block E, Rm EM3.3238, Montréal, Québec, H4A 3J1, Canada.
Nicole F BernardResearch Institute of the McGill University Health Center, Glen Site, 1001 Décarie Boulevard, Block E, Rm EM3.3238, Montréal, Québec, H4A 3J1, Canada. nicole.bernard@mcgill.ca.ORCID 0000-0001-5311-9409
McGill University Health Centre · CA

Funding

CIHR MOP-142494
6 · The paper itself

Abstract

backgroundNatural killer cell responses to virally-infected or transformed cells depend on the integration of signals received through inhibitory and activating natural killer cell receptors. Human Leukocyte Antigen null cells are used in vitro to stimulate natural killer cell activation through missing-self mechanisms. On the other hand, CEM.NKr.CCR5 cells are used to stimulate natural killer cells in an antibody dependent manner since they are resistant to direct killing by natural killer cells. Both K562 and 721.221 cell lines lack surface major histocompatibility compatibility complex class Ia ligands for inhibitory natural killer cell receptors. Previous work comparing natural killer cell stimulation by K562 and 721.221 found that they stimulated different frequencies of natural killer cell functional subsets. We hypothesized that natural killer cell function following K562, 721.221 or CEM.NKr.CCR5 stimulation reflected differences in the expression of ligands for activating natural killer cell receptors.

resultsK562 expressed a higher intensity of ligands for Natural Killer G2D and the Natural Cytotoxicity Receptors, which are implicated in triggering natural killer cell cytotoxicity. 721.221 cells expressed a greater number of ligands for activating natural killer cell receptors. 721.221 expressed cluster of differentiation 48, 80 and 86 with a higher mean fluorescence intensity than did K562. The only ligands for activating receptor that were detected on CEM.NKr.CCR5 cells at a high intensity were cluster of differentiation 48, and intercellular adhesion molecule-2.

conclusionsThe ligands expressed by K562 engage natural killer cell receptors that induce cytolysis. This is consistent with the elevated contribution that the cluster of differentiation 107a function makes to total K562 induced natural killer cell functionality compared to 721.221 cells. The ligands expressed on 721.221 cells can engage a larger number of activating natural killer cell receptors, which may explain their ability to activate a larger frequency of these cells to become functional and secrete cytokines. The few ligands for activating natural killer cell receptors expressed by CEM.NKr.CCR5 may reduce their ability to activate natural killer cells in an antibody independent manner explaining their relative resistance to direct natural killer cell cytotoxicity.

Indexed as

Gene ExpressionBiomarkersCell Line, TumorHLA AntigensHumansImmunophenotypingKiller Cells, NaturalLigandsLymphocyte ActivationReceptors, Natural Killer CellBiomarkersHLA AntigensLigandsReceptors, Natural Killer Cell721.221Activating NK receptor ligandsCEM.NKr.CCR5HLA null cellsK562NK cells

Identifiers

PMID30696399
PMCPMC6352444
OpenAlexW2921446662

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.