Evidence map›Paper›PMID 20923636›Full record

ArticleBiophysical journal2010

Activation or tolerance of natural killer cells is modulated by ligand quality in a nonmonotonic manner.

Jayajit Das

Open access · bronzeAbstract read
In one paragraph

Article in Biophysical journal, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

19 citing papers in PubMed, 39 citations in OpenAlex.

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  12. Enhancing network activation in natural killer cells: predictions from in silico modeling.Integrative biology : quantitative biosciences from nano to macro · 2020
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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

1 author at 1 institution in 1 country.

Jayajit DasBattelle Center for Mathematical Medicine, The Ohio State University, Columbus, OH, USA. das.70@osu.edu
Nationwide Children's Hospital · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Natural killer (NK) cells extend important immune resistance in vertebrates by lysing infected and tumor cells. A fine balance between opposing signals generated by a diverse set of stimulatory and inhibitory NK-cell receptors determines the fate of target cells interacting with the NK cells. We have developed a mathematical model involving membrane proximal initial signaling events that provides novel mechanistic insights into how activation of NK cells is modulated by the half-life of receptor-ligand interaction and ligand concentrations. We show that strong stimulatory ligands produce digital activation, whereas weaker stimulatory ligands can mediate inhibition by strengthening the signals generated by inhibitory ligands, as indicated in experiments in knockout mice. We find under certain conditions, counterintuitively, inhibitory receptors can help mediate activation instead of inhibition. Mechanistic insights gained from NK-cell signaling can facilitate understanding of complex signaling responses that occur due to cross talk between dueling signaling pathways in other cell types.

Indexed as

AnimalsEnzyme ActivationExtracellular Signal-Regulated MAP KinasesImmune ToleranceKiller Cells, NaturalLigandsLymphocyte ActivationMiceModels, ImmunologicalSignal TransductionExtracellular Signal-Regulated MAP KinasesLigands

Identifiers

PMID20923636
PMCPMC3042567
OpenAlexW2059259379

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.