Evidence map›Paper›PMID 40425090›Full record

ArticleMucosal immunology2025

MAIT cells exacerbate colonic inflammation in a genetically diverse murine model of spontaneous colitis.

Liyen Loh, David J Orlicky, Andrea Spengler, Joanne Domenico, Jared Klarquist, Cassandra Levens, Sofia Celli, Jennifer M Kofonow, Charles E Robertson, Olivier Lantz and 7 more

Abstract read
In one paragraph

Article in Mucosal immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Metabolic control of innate-like T cells.Nature reviews. Immunology · 2026
    Review
  8. Article
  9. Review
  10. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors.

Liyen LohDepartment of Immunology and Microbiology, University of Colorado School of Medicine, Aurora, CO, USA. Electronic address: liyen.loh@cuanschutz.edu.
David J OrlickyDepartment of Pathology, University of Colorado School of Medicine, Aurora, CO, USA.
Andrea SpenglerDepartment of Immunology and Microbiology, University of Colorado School of Medicine, Aurora, CO, USA.
Joanne DomenicoDepartment of Immunology and Microbiology, University of Colorado School of Medicine, Aurora, CO, USA.
Jared KlarquistDepartment of Immunology and Microbiology, University of Colorado School of Medicine, Aurora, CO, USA.
Cassandra LevensDivision of Rheumatology, Department of Medicine, University of Colorado School of Medicine, Aurora, CO, USA.
Sofia CelliDepartment of Biomedical Informatics, University of Colorado School of Medicine, Aurora, CO, USA.
Jennifer M KofonowDivision of Infectious Diseases, Department of Medicine, University of Colorado School of Medicine, Aurora, CO, USA.
Charles E RobertsonDivision of Infectious Diseases, Department of Medicine, University of Colorado School of Medicine, Aurora, CO, USA.
Olivier LantzInstitut Curie, Paris Sciences et Lettres University, Inserm U932, Immunity and Cancer, Paris, France.
Francois LegouxINSERM ERL 1305, CNRS UMR6290, Université de Rennes, Institut de Génétique & Développement de Rennes, France.
Daniel N FrankDivision of Infectious Diseases, Department of Medicine, University of Colorado School of Medicine, Aurora, CO, USA.
Jennifer MatsudaDepartment of Immunology and Microbiology, University of Colorado School of Medicine, Aurora, CO, USA; Mouse Genetics Core, National Jewish Health, Denver, CO, USA.
Paul J NormanDepartment of Immunology and Microbiology, University of Colorado School of Medicine, Aurora, CO, USA; Department of Biomedical Informatics, University of Colorado School of Medicine, Aurora, CO, USA.
Kristine A KuhnDivision of Rheumatology, Department of Medicine, University of Colorado School of Medicine, Aurora, CO, USA.
Joseph OnyiahDivision of Gastroenterology and Hepatology, Department of Medicine, University of Colorado School of Medicine, Aurora, CO, USA; Rocky Mountain Regional VA Medical Center, Aurora, CO, USA.
Laurent GapinDepartment of Immunology and Microbiology, University of Colorado School of Medicine, Aurora, CO, USA. Electronic address: laurent.gapin@cuanschutz.edu.

Funding

University of Colorado Cancer Center Support Grant - Lung Cancer Patient-Derived Xenografts with Autologous Human Immune SystemsP30CA046934 · NCI · UNIVERSITY OF COLORADO DENVER · PI James V Degregori · 1988 to 2026
$117.0M
Insights Into Immune-Related Diseases Born from Population GenomicsU01AI090905 · NIAID · UNIVERSITY OF COLORADO DENVER · PI Paul John Norman · 2010 to 2026
$10.9M
Role of MAIT cells in a mouse model of spontaneous colitisR21AI156003 · NIAID · UNIVERSITY OF COLORADO DENVER · PI GAPIN, LAURENT · 2021 to 2022
$428k
Transcriptional Regulation of Innate T cell fateR21AI163454 · NIAID · UNIVERSITY OF COLORADO DENVER · PI GAPIN, LAURENT · 2021 to 2022
$428k
BLRD VA IK2 BX003865NCI NIH HHS P30 CA046934NIAID NIH HHS R21 AI156003NIAID NIH HHS R21 AI163454NIAID NIH HHS U01 AI090905
6 · The paper itself

Abstract

IL-17-producing lymphocytes are involved in both tissue repair and the propagation of inflammation, with their effects highly context-dependent. Mucosal-Associated-Invariant-T-cells (MAIT), a subset of innate-like T cells with features of both Th1 and Th17 lineages, are increasingly recognized for their roles in mucosal immunity. Here, we identified the Collaborative-Cross CC011/Unc strain, which spontaneously develops chronic colitis, as being enriched for MAIT cells. This expansion coincides with an age-related loss of intestinal barrier permeability and colonic inflammation. Microbiota from CC011 mice activated MAIT cells in an MR1-dependent manner and selectively promoted the accumulation of MAIT17 cells in peripheral tissues. Single-cell transcriptomic analyses revealed colon MAIT cells from colitic CC011 mice expressed a pathogenic Th17-like signature, characterized by IL-1 and IL-23 signaling, IL-17A and IFNγ co-expression, and upregulation of IL-23R, features that correlated with inflammatory Ly6C

Indexed as

ColitisColonIntestinal MucosaMucosal-Associated Invariant T CellsTh17 CellsAnimalsCytokinesDisease Models, AnimalHumansInflammationMiceMice, Inbred C57BLMice, KnockoutCytokinesColitisInflammationMAIT cellsscRNAseq

Identifiers

PMID40425090
PMCPMC12439350

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.