Evidence map›Paper›PMID 32229721›Full record

ArticleThe Journal of clinical investigation2020

Microenvironmental Th9 and Th17 lymphocytes induce metastatic spreading in lung cancer.

Ylia Salazar, Xiang Zheng, David Brunn, Hartmann Raifer, Felix Picard, Yajuan Zhang, Hauke Winter, Stefan Guenther, Andreas Weigert, Benno Weigmann and 13 more

Abstract readVideo-Audio Media
In one paragraph

Article in The Journal of clinical investigation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 papers.

0numbers the graph read from it
0cells of the map it votes in
113citing papers in PubMed
–field-weighted citation impact
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

113 citing papers in PubMed.

  1. CD4Cell death & disease · 2022
    Trial
  2. Review
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  5. Contextualizing TNature reviews. Immunology · 2026
    Review
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53 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

23 authors.

Ylia SalazarMax Planck Institute for Heart and Lung Research, Department of Lung Development and Remodeling, member of the German Center for Lung Research (DZL), member of Cardio-Pulmonary Institute (CPI), Bad Nauheim, Germany.
Xiang ZhengMax Planck Institute for Heart and Lung Research, Department of Lung Development and Remodeling, member of the German Center for Lung Research (DZL), member of Cardio-Pulmonary Institute (CPI), Bad Nauheim, Germany.
David BrunnMax Planck Institute for Heart and Lung Research, Department of Lung Development and Remodeling, member of the German Center for Lung Research (DZL), member of Cardio-Pulmonary Institute (CPI), Bad Nauheim, Germany.
Hartmann RaiferInstitute for Medical Microbiology and.
Felix PicardInstitute for Medical Microbiology and.
Yajuan ZhangInstitute for Medical Microbiology and.
Hauke WinterTranslational Research Unit, Thoraxklinik at Heidelberg University, member of the DZL, Heidelberg, Germany.
Stefan GuentherBioinformatics and Deep Sequencing Platform, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.
Andreas WeigertInstitute of Biochemistry I, Faculty of Medicine, Goethe University Frankfurt, Frankfurt, Germany.
Benno WeigmannDepartment of Medicine 1, Friedrich-Alexander University Erlangen-Nuremberg, Erlangen, Germany.
Laure Dumoutierde Duve Institute, Université Catholique de Louvain, Brussels, Belgium.
Jean-Christophe Renauldde Duve Institute, Université Catholique de Louvain, Brussels, Belgium.
Ari WaismanInstitute for Molecular Medicine, University Medical Center of the Johannes Gutenberg University of Mainz, Mainz, Germany.
Anja SchmallMax Planck Institute for Heart and Lung Research, Department of Lung Development and Remodeling, member of the German Center for Lung Research (DZL), member of Cardio-Pulmonary Institute (CPI), Bad Nauheim, Germany.
Amanda TufmanRespiratory Medicine and Thoracic Oncology, Internal Medicine V, Ludwig-Maximilians-University of Munich and Thoracic Oncology Centre, member of the DZL, Munich, Germany.
Ludger FinkInstitute of Pathology and Cytology, Wetzlar, Germany.
Bernhard BrüneInstitute of Biochemistry I, Faculty of Medicine, Goethe University Frankfurt, Frankfurt, Germany.
Tobias BoppInstitute for Immunology, University Medical Center of the Johannes Gutenberg-University, Mainz, Germany. Research Center for Immunotherapy and University Medical Center, Johannes Gutenberg-University, Mainz, Germany. German Cancer Consortium, Heidelberg, Germany.
Friedrich GrimmingerDepartment of Internal Medicine, member of the DZL, member of CPI, Justus Liebig University, Giessen, Germany.
Werner SeegerMax Planck Institute for Heart and Lung Research, Department of Lung Development and Remodeling, member of the German Center for Lung Research (DZL), member of Cardio-Pulmonary Institute (CPI), Bad Nauheim, Germany.
Soni Savai PullamsettiMax Planck Institute for Heart and Lung Research, Department of Lung Development and Remodeling, member of the German Center for Lung Research (DZL), member of Cardio-Pulmonary Institute (CPI), Bad Nauheim, Germany.
Magdalena HuberInstitute for Medical Microbiology and.
Rajkumar SavaiMax Planck Institute for Heart and Lung Research, Department of Lung Development and Remodeling, member of the German Center for Lung Research (DZL), member of Cardio-Pulmonary Institute (CPI), Bad Nauheim, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immune microenvironment plays a critical role in lung cancer control versus progression and metastasis. In this investigation, we explored the effect of tumor-infiltrating lymphocyte subpopulations on lung cancer biology by studying in vitro cocultures, in vivo mouse models, and human lung cancer tissue. Lymphocyte conditioned media (CM) induced epithelial-mesenchymal transition (EMT) and migration in both primary human lung cancer cells and cell lines. Correspondingly, major accumulation of Th9 and Th17 cells was detected in human lung cancer tissue and correlated with poor survival. Coculturing lung cancer cells with Th9/Th17 cells or exposing them to the respective CM induced EMT in cancer cells and modulated the expression profile of genes implicated in EMT and metastasis. These features were reproduced by the signatory cytokines IL-9 and IL-17, with gene regulatory profiles evoked by these cytokines partly overlapping and partly complementary. Coinjection of Th9/Th17 cells with tumor cells in WT, Rag1-/-, Il9r-/-, and Il17ra-/- mice altered tumor growth and metastasis. Accordingly, inhibition of IL-9 or IL-17 cytokines by neutralizing antibodies decreased EMT and slowed lung cancer progression and metastasis. In conclusion, Th9 and Th17 lymphocytes induce lung cancer cell EMT, thereby promoting migration and metastatic spreading and offering potentially novel therapeutic strategies.

Indexed as

A549 CellsAnimalsCell MovementEpithelial-Mesenchymal TransitionHumansInterleukin-17Interleukin-9Lung NeoplasmsMiceNeoplasm MetastasisTh17 CellsTumor MicroenvironmentIL9 protein, humanInterleukin-17Interleukin-9CancerInflammationOncologyT cells

Identifiers

PMID32229721
PMCPMC7324180

What OpenQuestion holds

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Registered trials

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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.