Evidence map›Paper›PMID 29027233›Full record

ReviewImmunological reviews2017

Dysregulated cellular functions and cell stress pathways provide critical cues for activating and targeting natural killer cells to transformed and infected cells.

David H Raulet, Assaf Marcus, Laurent Coscoy

Open access · greenAbstract readReview
In one paragraph

Review in Immunological reviews, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

45 citing papers in PubMed, 61 citations in OpenAlex.

  1. DRP1 depletion protects NK cells from hypoxia-induced dysfunction.Redox report : communications in free radical research · 2026
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  15. Epigenetic and Immunological Features of Bladder Cancer.International journal of molecular sciences · 2023
    Review
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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

3 authors at 1 institution in 1 country.

David H RauletDepartment of Molecular and Cell Biology, Cancer Research Laboratory, Immunotherapy and Vaccine Research Initiative, University of California, Berkeley, Berkeley, CA, USA.ORCID 0000-0002-1257-8649
Assaf MarcusDepartment of Molecular and Cell Biology, Cancer Research Laboratory, Immunotherapy and Vaccine Research Initiative, University of California, Berkeley, Berkeley, CA, USA.
Laurent CoscoyDepartment of Molecular and Cell Biology, Cancer Research Laboratory, Immunotherapy and Vaccine Research Initiative, University of California, Berkeley, Berkeley, CA, USA.ORCID 0000-0002-7337-2345
University of California, Berkeley · US

Funding

EXPRESSION OF CLASS I-SPECIFIC RECEPTORS IN NK CELLSR01AI039642 · NIAID · UNIVERSITY OF CALIFORNIA BERKELEY · PI RAULET, DAVID H · 1996 to 2014
$4.9M
Role of NKG2D in immune responses to turmorsR01CA093678 · NCI · UNIVERSITY OF CALIFORNIA BERKELEY · PI RAULET, DAVID H · 2003 to 2019
$4.2M
STING-dependent activation of Natural Killer cells by viral and tumor DNAR01AI113041 · NIAID · UNIVERSITY OF CALIFORNIA BERKELEY · PI RAULET, DAVID H · 2014 to 2024
$4.1M
NCI NIH HHS R01 CA093678NIAID NIH HHS R01 AI039642NIAID NIH HHS R01 AI113041
6 · The paper itself

Abstract

Natural killer (NK) cells recognize and kill cancer cells and infected cells by engaging cell surface ligands that are induced preferentially or exclusively on these cells. These ligands are recognized by activating receptors on NK cells, such as NKG2D. In addition to activation by cell surface ligands, the acquisition of optimal effector activity by NK cells is driven in vivo by cytokines and other signals. This review addresses a developing theme in NK cell biology: that NK-activating ligands on cells, and the provision of cytokines and other signals that drive high effector function in NK cells, are driven by abnormalities that arise from transformation or the infected state. The pathways include genomic damage, which causes self DNA to be exposed in the cytosol of affected cells, where it activates the DNA sensor cGAS. The resulting signaling induces NKG2D ligands and also mobilizes NK cell activation. Other key pathways that regulate NKG2D ligands include PI-3 kinase activation, histone acetylation, and the integrated stress response. This review summarizes the roles of these pathways and their relevance in both viral infections and cancer.

Indexed as

AnimalsCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseCytotoxicity, ImmunologicDNA DamageHumansImmunologic SurveillanceInfectionsKiller Cells, NaturalLymphocyte ActivationNeoplasmsNK Cell Lectin-Like Receptor Subfamily KNucleotidyltransferasesPhosphatidylinositol 3-KinasesSignal TransductioncGAS protein, humanCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseNK Cell Lectin-Like Receptor Subfamily KNucleotidyltransferasesPhosphatidylinositol 3-Kinasescancercell stresscGAS-STINGinfectious diseasenatural killer cellsToll-like receptors/pattern recognition receptors

Identifiers

PMID29027233
PMCPMC5687887
OpenAlexW2761903097

What OpenQuestion holds

Textmetadata
LicenceTDM
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.