Evidence map›Paper›PMID 29264698›Full record

ReviewCancer immunology, immunotherapy : CII2018

Splice variants of human natural cytotoxicity receptors: novel innate immune checkpoints.

Avishai Shemesh, Michael Brusilovsky, Kiran Kundu, Aner Ottolenghi, Kerry S Campbell, Angel Porgador

Open access · greenAbstract readReview
In one paragraph

Review in Cancer immunology, immunotherapy : CII, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

11 citing papers in PubMed, 16 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

6 authors at 3 institutions in 2 countries.

Avishai ShemeshThe Shraga Segal Department of Microbiology, Immunology and Genetics, Goldman Building, Room 143, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer Sheva, 84105, Israel.
Michael BrusilovskyDivision of Allergy and Immunology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
Kiran KunduThe Shraga Segal Department of Microbiology, Immunology and Genetics, Goldman Building, Room 143, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer Sheva, 84105, Israel.
Aner OttolenghiThe Shraga Segal Department of Microbiology, Immunology and Genetics, Goldman Building, Room 143, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer Sheva, 84105, Israel.
Kerry S CampbellBlood Cell Development and Function Program, Institute for Cancer Research, Fox Chase Cancer Center, Philadelphia, PA, USA.
Angel PorgadorThe Shraga Segal Department of Microbiology, Immunology and Genetics, Goldman Building, Room 143, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer Sheva, 84105, Israel. angel@bgu.ac.il.
Ben-Gurion University of the Negev · ILCincinnati Children's Hospital Medical Center · USFox Chase Cancer Center · US

Funding

Israeli Ministry of Science and Technology/German Cancer Research Center program Grant CA172Israeli Ministry of Science and Technology grant 54180Israel Science Foundation 1188/16United States - Israel Binational Science Foundation 2015344
6 · The paper itself

Abstract

The natural cytotoxicity receptors (NCRs; NKp30, NKp44, and NKp46) were first defined as activating receptors on human NK cells that are important in recognition of and response to tumors. A flurry of recent research, however, has revealed that differential splicing can occur during transcription of each of the NCR genes, resulting in some transcripts that encode receptor isoforms with inhibitory functions. These alternative transcripts can arise in certain tissue microenvironments and appear to be induced by cytokines. Evidence indicates that some of the inhibitory NCRs are triggered by specific ligands, such as the interaction of the inhibitory isoform of NKp44 with PCNA on the surface of tumor cells. Here, we review the different NCR splice variants, cytokines that modulate their expression, their functional impacts on innate immune cells, and their differential expression in the contexts of cancer, pregnancy, and infections. The recent discovery of these inhibitory NCR isoforms has revealed novel innate immune checkpoints, many of which still lack defined ligands and clear mechanisms driving their expression. These NCR checkpoint pathways offer exciting potential therapeutic targets to manipulate innate immune functions under defined pathological conditions, such as cancer, pregnancy disorders, and pathogen exposure.

Indexed as

Alternative SplicingAnimalsCellular MicroenvironmentCytotoxicity, ImmunologicGene Expression ProfilingGene Expression RegulationHumansImmunity, InnateReceptors, ImmunologicReceptors, ImmunologicImmune checkpointsIsoformsNKp30NKp44NKp46Splice variants

Identifiers

PMID29264698
PMCPMC11028282
OpenAlexW2780697849

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.