Evidence map›Paper›PMID 32451418›Full record

ArticleNature communications2020

TGF-β signaling in Th17 cells promotes IL-22 production and colitis-associated colon cancer.

Laura Garcia Perez, Jan Kempski, Heather M McGee, Penelope Pelzcar, Theodora Agalioti, Anastasios Giannou, Leonie Konczalla, Leonie Brockmann, Ramez Wahib, Hao Xu and 14 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 104 papers.

0numbers the graph read from it
0cells of the map it votes in
104citing papers in PubMed
7.5field-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

104 citing papers in PubMed, 144 citations in OpenAlex.

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44 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

24 authors at 6 institutions in 3 countries.

Laura Garcia PerezI. Department of Medicine, University Medical Center Hamburg-Eppendorf, 20246, Hamburg, Germany.
Jan KempskiI. Department of Medicine, University Medical Center Hamburg-Eppendorf, 20246, Hamburg, Germany.
Heather M McGeeCenter for Immunobiology and Microbial Pathogenesis, Salk Institute for Biological Studies, 10010, La Jolla, CA, USA.ORCID http://orcid.org/0000-0003-3761-5087
Penelope PelzcarI. Department of Medicine, University Medical Center Hamburg-Eppendorf, 20246, Hamburg, Germany.
Theodora AgaliotiDepartment of General, Visceral and Thoracic Surgery, University Medical Center Hamburg-Eppendorf, 20246, Hamburg, Germany.
Anastasios GiannouI. Department of Medicine, University Medical Center Hamburg-Eppendorf, 20246, Hamburg, Germany.
Leonie KonczallaDepartment of General, Visceral and Thoracic Surgery, University Medical Center Hamburg-Eppendorf, 20246, Hamburg, Germany.ORCID http://orcid.org/0000-0001-7674-1276
Leonie BrockmannDepartment of Microbiology and Immunology, Columbia University, New York, NY, USA.
Ramez WahibDepartment of General, Visceral and Thoracic Surgery, University Medical Center Hamburg-Eppendorf, 20246, Hamburg, Germany.ORCID http://orcid.org/0000-0002-2545-8160
Hao XuDepartment of Immunobiology, School of Medicine, Yale University, New Haven, CT, 06520, USA.
Maria Carolina Amezcua VeselyDepartment of Immunobiology, School of Medicine, Yale University, New Haven, CT, 06520, USA.
Shiwa SoukouI. Department of Medicine, University Medical Center Hamburg-Eppendorf, 20246, Hamburg, Germany.
Babett SteglichI. Department of Medicine, University Medical Center Hamburg-Eppendorf, 20246, Hamburg, Germany.
Tanja BedkeI. Department of Medicine, University Medical Center Hamburg-Eppendorf, 20246, Hamburg, Germany.
Carolin MantheyI. Department of Medicine, University Medical Center Hamburg-Eppendorf, 20246, Hamburg, Germany.
Oliver SeizI. Department of Medicine, University Medical Center Hamburg-Eppendorf, 20246, Hamburg, Germany.
Björn-Philipp DiercksDepartment of Biochemistry and Molecular Cell Biology, University Medical Center Hamburg-Eppendorf, 20246, Hamburg, Germany.ORCID http://orcid.org/0000-0002-6635-1706
Stylianos GnafakisLaboratory of Innate Immunity, Department of Microbiology, Infectious Diseases and Immunology, Charité - Universitätsmedizin Berlin, Hindenburgdamm 30, 12203, Berlin, Germany.
Andreas H GuseDepartment of Biochemistry and Molecular Cell Biology, University Medical Center Hamburg-Eppendorf, 20246, Hamburg, Germany.ORCID http://orcid.org/0000-0002-3972-401X
Daniel PerezDepartment of General, Visceral and Thoracic Surgery, University Medical Center Hamburg-Eppendorf, 20246, Hamburg, Germany.
Jakob R IzbickiDepartment of General, Visceral and Thoracic Surgery, University Medical Center Hamburg-Eppendorf, 20246, Hamburg, Germany.
Nicola GaglianiI. Department of Medicine, University Medical Center Hamburg-Eppendorf, 20246, Hamburg, Germany.
Richard A Flavell *Department of Immunobiology, School of Medicine, Yale University, New Haven, CT, 06520, USA. richard.flavell@yale.edu.ORCID http://orcid.org/0000-0003-4461-0778
Samuel Huber *I. Department of Medicine, University Medical Center Hamburg-Eppendorf, 20246, Hamburg, Germany. shuber@uke.de.ORCID http://orcid.org/0000-0001-9325-8227
Universität Hamburg · DEYale University · USColumbia University · USGerman Rheumatism Research Centre · DEHoward Hughes Medical Institute · USSalk Institute for Biological Studies · US

Funding

Yale Clinical and Translational Science Award (U Component)UL1TR001863 · NCATS · YALE UNIVERSITY · PI John H. Krystal, LUCILA OHNO-MACHADO · 2016 to 2026
$102.9M
Howard Hughes Medical InstituteNCATS NIH HHS UL1 TR001863
6 · The paper itself

Abstract

IL-22 has dual functions during tumorigenesis. Short term IL-22 production protects against genotoxic stress, whereas uncontrolled IL-22 activity promotes tumor growth; therefore, tight regulation of IL-22 is essential. TGF-β1 promotes the differentiation of Th17 cells, which are known to be a major source of IL-22, but the effect of TGF-β signaling on the production of IL-22 in CD4+ T cells is controversial. Here we show an increased presence of IL-17+IL-22+ cells and TGF-β1 in colorectal cancer compared to normal adjacent tissue, whereas the frequency of IL-22 single producing cells is not changed. Accordingly, TGF-β signaling in CD4+ T cells (specifically Th17 cells) promotes the emergence of IL-22-producing Th17 cells and thereby tumorigenesis in mice. IL-22 single producing T cells, however, are not dependent on TGF-β signaling. We show that TGF-β, via AhR induction, and PI3K signaling promotes IL-22 production in Th17 cells.

Indexed as

AnimalsBasic Helix-Loop-Helix ProteinsCarcinogenesisCell DifferentiationColitisColonic NeoplasmsColorectal NeoplasmsDisease Models, AnimalFemaleHumansInterleukin-17Interleukin-22InterleukinsLymphocytes, Tumor-InfiltratingMaleMiceAhr protein, mouseBasic Helix-Loop-Helix ProteinsIl17a protein, mouseInterleukin-17Interleukin-22InterleukinsPhosphatidylinositol 3-KinasesReceptors, Aryl HydrocarbonTGFB1 protein, humanTransforming Growth Factor betaTransforming Growth Factor beta1

Identifiers

PMID32451418
PMCPMC7248087
OpenAlexW3026251363

What OpenQuestion holds

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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.