Evidence map›Paper›PMID 28300057›Full record

ArticleNature communications2017

Combined toll-like receptor 3/7/9 deficiency on host cells results in T-cell-dependent control of tumour growth.

Johanna C Klein, Katrin Moses, Gennadiy Zelinskyy, Simon Sody, Jan Buer, Stephan Lang, Iris Helfrich, Ulf Dittmer, Carsten J Kirschning, Sven Brandau

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

18 citing papers in PubMed, 36 citations in OpenAlex.

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  11. Pathogen Molecular Pattern Receptor Agonists: Treating Cancer by Mimicking Infection.Clinical cancer research : an official journal of the American Association for Cancer Research · 2019
    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

10 authors at 2 institutions in 1 country.

Johanna C KleinResearch Division of the Department of Otorhinolaryngology, University Hospital Essen, University Duisburg-Essen, Hufelandstrasse 55, D-45122 Essen, Germany.
Katrin MosesResearch Division of the Department of Otorhinolaryngology, University Hospital Essen, University Duisburg-Essen, Hufelandstrasse 55, D-45122 Essen, Germany.
Gennadiy ZelinskyyInstitute of Virology, University Hospital Essen, University Duisburg-Essen, D-45122 Essen, Germany.
Simon SodyResearch Division of the Department of Otorhinolaryngology, University Hospital Essen, University Duisburg-Essen, Hufelandstrasse 55, D-45122 Essen, Germany.
Jan BuerInstitute of Medical Microbiology, University Hospital Essen, University Duisberg-Essen, D-45122 Essen, Germany.
Stephan LangResearch Division of the Department of Otorhinolaryngology, University Hospital Essen, University Duisburg-Essen, Hufelandstrasse 55, D-45122 Essen, Germany.
Iris HelfrichGerman Cancer Consortium (DKTK), D-45122 Essen, Germany.
Ulf DittmerInstitute of Virology, University Hospital Essen, University Duisburg-Essen, D-45122 Essen, Germany.
Carsten J KirschningInstitute of Medical Microbiology, University Hospital Essen, University Duisberg-Essen, D-45122 Essen, Germany.
Sven BrandauResearch Division of the Department of Otorhinolaryngology, University Hospital Essen, University Duisburg-Essen, Hufelandstrasse 55, D-45122 Essen, Germany.
University of Duisburg-Essen · DEDeutschen Konsortium für Translationale Krebsforschung · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Toll-like receptors (TLRs) are located either on the cell surface or intracellularly in endosomes and their activation normally contributes to the induction of protective immune responses. However, in cancer their activation by endogenous ligands can modulate tumour progression. It is currently unknown how endosomal TLRs regulate endogenous anti-tumour immunity. Here we show that TLR3, 7 and 9 deficiencies on host cells, after initial tumour growth, result in complete tumour regression and induction of anti-tumour immunity. Tumour regression requires the combined absence of all three receptors, is dependent on both CD4 and CD8 T cells and protects the mice from subsequent tumour challenge. While tumours in control mice are infiltrated by higher numbers of regulatory T cells, tumour regression in TLR-deficient mice is paralleled by altered vascular structure and strongly induced influx of cytotoxic and cytokine-producing effector T cells. Thus, endosomal TLRs may represent a molecular link between the inflamed tumour cell phenotype, anti-tumour immunity and the regulation of T-cell activation.

Indexed as

Tumor MicroenvironmentAnimalsCell Line, TumorEndosomesFemaleMice, Inbred C57BLMice, KnockoutNeoplasms, ExperimentalT-LymphocytesToll-Like ReceptorsToll-Like Receptors

Identifiers

PMID28300057
PMCPMC5356072
OpenAlexW2595035620

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.