Evidence map›Paper›PMID 25149452›Full record

ArticleeLife2014

Recognition of tumor cells by Dectin-1 orchestrates innate immune cells for anti-tumor responses.

Shiho Chiba, Hiroaki Ikushima, Hiroshi Ueki, Hideyuki Yanai, Yoshitaka Kimura, Sho Hangai, Junko Nishio, Hideo Negishi, Tomohiko Tamura, Shinobu Saijo and 2 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in eLife, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 papers.

0numbers the graph read from it
0cells of the map it votes in
117citing papers in PubMed
6.8field-weighted citation impact, top 2% 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

117 citing papers in PubMed, 215 citations in OpenAlex.

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  11. The C-Type Lectin Receptors.Advances in experimental medicine and biology · 2025
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57 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 5 institutions in 1 country.

Shiho ChibaDepartment of Molecular Immunology, Institute of Industrial Science, The University of Tokyo, Tokyo, Japan.
Hiroaki IkushimaDepartment of Molecular Immunology, Institute of Industrial Science, The University of Tokyo, Tokyo, Japan.
Hiroshi UekiDepartment of Molecular Immunology, Institute of Industrial Science, The University of Tokyo, Tokyo, Japan.
Hideyuki YanaiDepartment of Molecular Immunology, Institute of Industrial Science, The University of Tokyo, Tokyo, Japan.
Yoshitaka KimuraDepartment of Molecular Immunology, Institute of Industrial Science, The University of Tokyo, Tokyo, Japan.
Sho HangaiDepartment of Molecular Immunology, Institute of Industrial Science, The University of Tokyo, Tokyo, Japan.
Junko NishioDepartment of Molecular Immunology, Institute of Industrial Science, The University of Tokyo, Tokyo, Japan.
Hideo NegishiDepartment of Molecular Immunology, Institute of Industrial Science, The University of Tokyo, Tokyo, Japan.
Tomohiko TamuraDepartment of Immunology, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Shinobu SaijoDepartment of Molecular Immunology, Medical Mycology Research Center, Chiba University, Chiba, Japan.
Yoichiro IwakuraCenter for Animal Disease Models, Research Institute for Biomedical Sciences, Tokyo University of Science, Noda, Japan.
Tadatsugu TaniguchiDepartment of Molecular Immunology, Institute of Industrial Science, The University of Tokyo, Tokyo, Japan.
The University of Tokyo · JPChiba University · JPJapan Science and Technology Agency · JPTokyo University of Science · JPYokohama City University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The eradication of tumor cells requires communication to and signaling by cells of the immune system. Natural killer (NK) cells are essential tumor-killing effector cells of the innate immune system; however, little is known about whether or how other immune cells recognize tumor cells to assist NK cells. Here, we show that the innate immune receptor Dectin-1 expressed on dendritic cells and macrophages is critical to NK-mediated killing of tumor cells that express N-glycan structures at high levels. Receptor recognition of these tumor cells causes the activation of the IRF5 transcription factor and downstream gene induction for the full-blown tumoricidal activity of NK cells. Consistent with this, we show exacerbated in vivo tumor growth in mice genetically deficient in either Dectin-1 or IRF5. The critical contribution of Dectin-1 in the recognition of and signaling by tumor cells may offer new insight into the anti-tumor immune system with therapeutic implications.

Indexed as

AnimalsCell CommunicationCell Line, TumorCell ProliferationCytotoxicity, ImmunologicDectin-1Dendritic CellsGene Expression Regulation, NeoplasticHEK293 CellsHumansImmunity, InnateInterferon Regulatory FactorsKiller Cells, NaturalLectins, C-TypeMacrophagesMelanoma, ExperimentalDectin-1Interferon Regulatory FactorsIrf5 protein, mouseLectins, C-TypePolysaccharidesRNA, MessengerDectin-1immunologyinnate immunityIRFmouseNK cell

Identifiers

PMID25149452
PMCPMC4161974
OpenAlexW2117845120

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.