Evidence map›Paper›PMID 27384869›Full record

ArticleCancer science2016

IL-17A-producing CD30(+) Vδ1 T cells drive inflammation-induced cancer progression.

Yoshitaka Kimura, Nao Nagai, Naoki Tsunekawa, Marimo Sato-Matsushita, Takayuki Yoshimoto, Daniel J Cua, Yoichiro Iwakura, Hideo Yagita, Futoshi Okada, Hideaki Tahara and 3 more

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

22 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
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  7. γδ T cells: origin and fate, subsets, diseases and immunotherapy.Signal transduction and targeted therapy · 2023
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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

13 authors at 7 institutions in 2 countries.

Yoshitaka KimuraLaboratory of Cancer Biology and Molecular Immunology, Graduate School of Pharmaceutical Sciences, University of Tokyo, Bunkyo-ku, Tokyo, Japan.
Nao NagaiLaboratory of Cancer Biology and Molecular Immunology, Graduate School of Pharmaceutical Sciences, University of Tokyo, Bunkyo-ku, Tokyo, Japan.
Naoki TsunekawaLaboratory of Cancer Biology and Molecular Immunology, Graduate School of Pharmaceutical Sciences, University of Tokyo, Bunkyo-ku, Tokyo, Japan.
Marimo Sato-MatsushitaDepartment of Surgery and Bioengineering, Institute of Medical Science, University of Tokyo, Minato-ku, Tokyo, Japan.
Takayuki YoshimotoDepartment of Immunoregulation, Institute of Medical Science, Tokyo Medical University, Shinjuku-ku, Tokyo, Japan.
Daniel J CuaPathway Biology, Merck Research Laboratories, Palo Alto, California, USA.
Yoichiro IwakuraCenter for Animal Disease Models, Research Institute for Biomedical Sciences, Tokyo University of Science, Noda, Chiba, Japan.
Hideo YagitaDepartment of Immunology, Juntendo University School of Medicine, Bunkyo-ku, Tokyo, Japan.
Futoshi OkadaDivision of Pathological Biochemistry, Tottori University Faculty of Medicine, Yonago, Tottori, Japan.
Hideaki TaharaDepartment of Surgery and Bioengineering, Institute of Medical Science, University of Tokyo, Minato-ku, Tokyo, Japan.
Ikuo SaikiDivision of Pathogenic Biochemistry, Department of Bioscience, Institute of Natural Medicine, University of Toyama, Toyama, Toyama, Japan.
Tatsuro IrimuraLaboratory of Cancer Biology and Molecular Immunology, Graduate School of Pharmaceutical Sciences, University of Tokyo, Bunkyo-ku, Tokyo, Japan.
Yoshihiro HayakawaLaboratory of Cancer Biology and Molecular Immunology, Graduate School of Pharmaceutical Sciences, University of Tokyo, Bunkyo-ku, Tokyo, Japan. haya@inm.u-toyama.ac.jp.
The University of Tokyo · JPTokyo University of Science · JPJuntendo University · JPMerck & Co., Inc., Rahway, NJ, USA (United States) · USTokyo Medical University · JPTottori University · JPUniversity of Toyama · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although it has been suspected that inflammation is associated with increased tumor metastasis, the exact type of immune response required to initiate cancer progression and metastasis remains unknown. In this study, by using an in vivo tumor progression model in which low tumorigenic cancer cells acquire malignant metastatic phenotype after exposure to inflammation, we found that IL-17A is a critical cue for escalating cancer cell malignancy. We further demonstrated that the length of exposure to an inflammatory microenvironment could be associated with acquiring greater tumorigenicity and that IL-17A was critical for amplifying such local inflammation, as observed in the production of IL-1β and neutrophil infiltration following the cross-talk between cancer and host stromal cells. We further determined that γδT cells expressing Vδ1 semi-invariant TCR initiate cancer-promoting inflammation by producing IL-17A in an MyD88/IL-23-dependent manner. Finally, we identified CD30 as a key molecule in the inflammatory function of Vδ1T cells and the blockade of this pathway targeted this cancer immune-escalation process. Collectively, these results reveal the importance of IL-17A-producing CD30(+) Vδ1T cells in triggering inflammation and orchestrating a microenvironment leading to cancer progression.

Indexed as

AnimalsCell Line, TumorDisease Models, AnimalDisease ProgressionImmunityInflammationInterleukin-17Ki-1 AntigenMiceMice, KnockoutModels, BiologicalNeoplasmsT-Lymphocyte SubsetsTumor MicroenvironmentInterleukin-17Ki-1 AntigenCD30IL-17IL-1βneutrophilγδ T cell

Identifiers

PMID27384869
PMCPMC5021032
OpenAlexW2460443320

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.