Evidence map›Paper›PMID 41317905›Full record

ArticleMucosal immunology2026

ILC3s mediate intestinal immune-epithelial interactions via TGF-β1 activation.

Diana Coman, John W Bassett, Isabelle Coales, Ainize Peña-Cearra, Emily Read, Emma H Kromann, Daniel Brice, Zuzanna Łukasik, Helena Paidassi, Matthew R Hepworth and 5 more

Abstract read
In one paragraph

Article in Mucosal immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
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

15 authors.

Diana ComanCentre for Host-Microbiome Interactions, King's College London, London, United Kingdom.
John W BassettCenter for Infectious Medicine, Department of Medicine Huddinge, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden.
Isabelle CoalesCentre for Host-Microbiome Interactions, King's College London, London, United Kingdom.
Ainize Peña-CearraCentre for Host-Microbiome Interactions, King's College London, London, United Kingdom; Department of Immunology, Microbiology and Parasitology, Faculty of Medicine and Nursing, University of the Basque Country (EHU), Bilbao, Spain.
Emily ReadCentre for Host-Microbiome Interactions, King's College London, London, United Kingdom; The Blizard Institute, Queen Mary University London, London, United Kingdom.
Emma H KromannCentre for Host-Microbiome Interactions, King's College London, London, United Kingdom.
Daniel BriceLydia Becker Institute of Immunology and Inflammation, University of Manchester, Manchester, United Kingdom; Wellcome Trust Centre for Cell-Matrix Research, University of Manchester, Manchester, United Kingdom; Division of Immunology, Immunity to Infection and Respiratory Medicine, Faculty of Biology, Medicine and Health, Manchester Academic Health Sciences Centre, University of Manchester, Manchester, United Kingdom.
Zuzanna ŁukasikDepartment for Inflammation Biology, School of Immunology & Microbial Sciences, King's College London, London, United Kingdom; Department of Rheumatology, Faculty of Medicine and Health Sciences, Ghent University and Unit for Molecular Immunology and Inflammation, VIB-UGent Center for Inflammation Research, Ghent, Belgium.
Helena PaidassiCentre International de Recherche en Infectiologie (CIRI), Univ Lyon, Inserm, U1111 Université Claude Bernard Lyon 1, CNRS, ENS de Lyon, Lyon, France.
Matthew R HepworthLydia Becker Institute of Immunology and Inflammation, University of Manchester, Manchester, United Kingdom; Division of Immunology, Immunity to Infection and Respiratory Medicine, Faculty of Biology, Medicine and Health, Manchester Academic Health Sciences Centre, University of Manchester, Manchester, United Kingdom.
Robin J DartDepartment for Inflammation Biology, School of Immunology & Microbial Sciences, King's College London, London, United Kingdom; Immunosurveillance Laboratory, The Francis Crick Institute, London, United Kingdom; Department of Gastroenterology, Guy's and St Thomas' Foundation Trust, London, United Kingdom.
Mark A TravisLydia Becker Institute of Immunology and Inflammation, University of Manchester, Manchester, United Kingdom; Wellcome Trust Centre for Cell-Matrix Research, University of Manchester, Manchester, United Kingdom; Division of Immunology, Immunity to Infection and Respiratory Medicine, Faculty of Biology, Medicine and Health, Manchester Academic Health Sciences Centre, University of Manchester, Manchester, United Kingdom.
Jenny MjösbergCenter for Infectious Medicine, Department of Medicine Huddinge, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden; Clinical Lung- and Allergy Research Unit, Department of Medicine Huddinge, Karolinska Institutet, Stockholm, Sweden; The Department of Respiratory Medicine and Allergy, Karolinska University Hospital Huddinge, Stockholm, Sweden.
Luke B RobertsLydia Becker Institute of Immunology and Inflammation, University of Manchester, Manchester, United Kingdom; Division of Immunology, Immunity to Infection and Respiratory Medicine, Faculty of Biology, Medicine and Health, Manchester Academic Health Sciences Centre, University of Manchester, Manchester, United Kingdom.
Joana F NevesCentre for Host-Microbiome Interactions, King's College London, London, United Kingdom. Electronic address: joana.pereira_das_neves@kcl.ac.uk.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammatory Bowel Disease (IBD) is a chronic inflammatory condition affecting the gastrointestinal tract. It is characterised by epithelial and immunological dysfunctions, including alterations in populations of Innate Lymphoid Cells (ILCs), including tissue-resident RORγt-expressing Group 3 ILCs (ILC3s). ILC3s contribute to the maintenance of intestinal homeostasis by closely interacting with both the epithelium and adaptive immune cells. Here, we reveal that murine and human ILC3s modulate these interactions through Transforming Growth Factor-Beta 1 (TGF-β1), a pleiotropic cytokine secreted in an inactive form. We show that ILC3s synthesise and activate latent TGF-β1 through mechanical and proteolytic pathways. ILC3s aid the induction of FoxP3

Indexed as

Inflammatory Bowel DiseasesIntestinal MucosaLymphocytesT-Lymphocytes, RegulatoryTransforming Growth Factor beta1AnimalsCell CommunicationForkhead Transcription FactorsHomeostasisHumansImmunity, InnateMiceMice, Inbred C57BLSignal TransductionForkhead Transcription FactorsTransforming Growth Factor beta1ILC3Innate Lymphoid CellsIntestineOrganoidsRegulatory T cellsTGF-β1

Identifiers

PMID41317905
PMCPMC13195368

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.