Evidence map›Paper›PMID 32747815›Full record

ArticleNature immunology2020

ILC2-driven innate immune checkpoint mechanism antagonizes NK cell antimetastatic function in the lung.

Martijn J Schuijs, Shaun Png, Arianne C Richard, Anastasia Tsyben, Gregory Hamm, Julie Stockis, Celine Garcia, Silvain Pinaud, Ashley Nicholls, Xavier Romero Ros and 13 more

Open access · greenAbstract read
In one paragraph

Article in Nature immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 115 papers.

0numbers the graph read from it
0cells of the map it votes in
115citing papers in PubMed
8.7field-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

115 citing papers in PubMed, 155 citations in OpenAlex.

  1. Article
  2. Tissue adaptation of eosinophils.Journal of leukocyte biology · 2026
    Review
  3. Review
  4. ILC2s and their immune checkpoints in the antitumor response.Journal for immunotherapy of cancer · 2026
    Review
  5. IDH1 Mutant Glioma Favors Group 3 Innate Lymphoid Cells and Is Resistant to Immune Checkpoint Expression.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  6. Article
  7. Article
  8. Involvement of increased arginase-1The Journal of international medical research · 2026
    Article
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55 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 at 6 institutions in 2 countries.

Martijn J SchuijsCRUK Cambridge Institute, University of Cambridge, Cambridge, UK.
Shaun PngCRUK Cambridge Institute, University of Cambridge, Cambridge, UK.ORCID http://orcid.org/0000-0002-2364-4621
Arianne C RichardCRUK Cambridge Institute, University of Cambridge, Cambridge, UK.ORCID http://orcid.org/0000-0002-8708-9997
Anastasia TsybenCRUK Cambridge Institute, University of Cambridge, Cambridge, UK.
Gregory HammImaging and Data Analytics, Clinical Pharmacology and Safety Sciences, BioPharmaceuticals R&D, AstraZeneca, Cambridge, UK.
Julie StockisCRUK Cambridge Institute, University of Cambridge, Cambridge, UK.ORCID http://orcid.org/0000-0003-4911-6891
Celine GarciaCRUK Cambridge Institute, University of Cambridge, Cambridge, UK.
Silvain PinaudCRUK Cambridge Institute, University of Cambridge, Cambridge, UK.ORCID http://orcid.org/0000-0002-9541-3611
Ashley NichollsCRUK Cambridge Institute, University of Cambridge, Cambridge, UK.
Xavier Romero RosBioscience Asthma, Research and Early Development, Respiratory & Immunology, BioPharmaceuticals R&D, AstraZeneca, Cambridge, UK.
Jing SuCRUK Cambridge Institute, University of Cambridge, Cambridge, UK.
Matthew D EldridgeCRUK Cambridge Institute, University of Cambridge, Cambridge, UK.ORCID http://orcid.org/0000-0002-5799-8911
Angela RiedelMRC Cancer Unit, University of Cambridge, Cambridge, UK.
Eva M SerraoCRUK Cambridge Institute, University of Cambridge, Cambridge, UK.ORCID http://orcid.org/0000-0002-1402-3444
Hans-Reimer RodewaldDivision of Cellular Immunology, German Cancer Research Center, Heidelberg, Germany.
Matthias MackDepartment of Internal Medicine, University Hospital Regensburg, Regensburg, Germany.
Jacqueline D ShieldsMRC Cancer Unit, University of Cambridge, Cambridge, UK.ORCID http://orcid.org/0000-0003-2153-9710
E Suzanne CohenBioscience Asthma, Research and Early Development, Respiratory & Immunology, BioPharmaceuticals R&D, AstraZeneca, Cambridge, UK.
Andrew N J McKenzieMRC Laboratory of Molecular Biology, Cambridge, UK.
Richard J A GoodwinImaging and Data Analytics, Clinical Pharmacology and Safety Sciences, BioPharmaceuticals R&D, AstraZeneca, Cambridge, UK.ORCID http://orcid.org/0000-0001-5699-8488
Kevin M BrindleCRUK Cambridge Institute, University of Cambridge, Cambridge, UK.
John C MarioniCRUK Cambridge Institute, University of Cambridge, Cambridge, UK.
Timotheus Y F HalimCRUK Cambridge Institute, University of Cambridge, Cambridge, UK. Tim.Halim@cruk.cam.ac.uk.ORCID http://orcid.org/0000-0001-9773-0023
University of Cambridge · GBAstraZeneca (United Kingdom) · GBEuropean Bioinformatics Institute · GBGerman Cancer Research Center · DEMRC Laboratory of Molecular Biology · GBUniversity Hospital Regensburg · DE

Funding

Cancer Research UK 22231Cancer Research UK 24995Cancer Research UK 28289Cancer Research UK A24995Cancer Research UK C197/A25040Medical Research Council MC_U105178805Medical Research Council MC_UP_1101/2Medical Research Council MC_UU_12022/5Medical Research Council MR/P014178/1Wellcome Trust 204622
6 · The paper itself

Abstract

Metastasis constitutes the primary cause of cancer-related deaths, with the lung being a commonly affected organ. We found that activation of lung-resident group 2 innate lymphoid cells (ILC2s) orchestrated suppression of natural killer (NK) cell-mediated innate antitumor immunity, leading to increased lung metastases and mortality. Using multiple models of lung metastasis, we show that interleukin (IL)-33-dependent ILC2 activation in the lung is involved centrally in promoting tumor burden. ILC2-driven innate type 2 inflammation is accompanied by profound local suppression of interferon-γ production and cytotoxic function of lung NK cells. ILC2-dependent suppression of NK cells is elaborated via an innate regulatory mechanism, which is reliant on IL-5-induced lung eosinophilia, ultimately limiting the metabolic fitness of NK cells. Therapeutic targeting of IL-33 or IL-5 reversed NK cell suppression and alleviated cancer burden. Thus, we reveal an important function of IL-33 and ILC2s in promoting tumor metastasis via their capacity to suppress innate type 1 immunity.

Indexed as

AnimalsCell Line, TumorCytotoxicity, ImmunologicEosinophilsHumansImmune ToleranceImmunity, InnateInterleukin-33Interleukin-5Killer Cells, NaturalLungLung NeoplasmsLymphocytesMiceMice, Inbred BALB CMice, Inbred C57BLInterleukin-33Interleukin-5

Identifiers

PMID32747815
PMCPMC7116357
OpenAlexW3046993567

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.