Evidence map›Paper›PMID 38310974›Full record

ArticleThe Journal of allergy and clinical immunology2024

Epithelial overexpression of IL-33 induces eosinophilic esophagitis dependent on IL-13.

Mia Y Masuda, Grace C Pyon, Huijun Luo, William E LeSuer, Arina Putikova, Adelyn Dao, Danna R Ortiz, Aliviya R Schulze, Nicholas Fritz, Takao Kobayashi and 11 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of allergy and clinical immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
13.7field-weighted citation impact, top 1% 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

27 citing papers in PubMed, 24 citations in OpenAlex.

  1. Eosinophilic gastrointestinal diseases.Nature reviews. Disease primers · 2026
    Review
  2. Bidirectional risk of autoimmune disease and eosinophilic esophagitis in Sweden.Esophagus : official journal of the Japan Esophageal Society · 2026
    Article
  3. Review
  4. Article
  5. Review
  6. Oesophageal Epithelial Cell-Intrinsic MHCII Regulates Food Antigen-Dependent Eosinophilic Esophagitis in an IFNγ-Dependent Manner.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2026
    Article
  7. PSMB8 stratifies therapy response in eosinophilic esophagitis.Clinical and experimental immunology · 2026
    Article
  8. Review
  9. Review
  10. Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. The oesophagus as an immune organ.Nature reviews. Gastroenterology & hepatology · 2025
    Review
  18. Mouse models of eosinophilic esophagitis: molecular and translational insights.American journal of physiology. Gastrointestinal and liver physiology · 2025
    Review
  19. Article
  20. 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

21 authors at 6 institutions in 1 country.

Mia Y MasudaDivision of Allergy, Asthma, and Clinical Immunology, Department of Medicine, Mayo Clinic Arizona, Scottsdale, Ariz; Department of Immunology, Mayo Clinic, Rochester, and Mayo Clinic Arizona, Scottsdale, Ariz.
Grace C PyonDivision of Allergy, Asthma, and Clinical Immunology, Department of Medicine, Mayo Clinic Arizona, Scottsdale, Ariz.
Huijun LuoDivision of Allergy, Asthma, and Clinical Immunology, Department of Medicine, Mayo Clinic Arizona, Scottsdale, Ariz.
William E LeSuerDivision of Allergy, Asthma, and Clinical Immunology, Department of Medicine, Mayo Clinic Arizona, Scottsdale, Ariz.
Arina PutikovaDivision of Allergy, Asthma, and Clinical Immunology, Department of Medicine, Mayo Clinic Arizona, Scottsdale, Ariz.
Adelyn DaoDivision of Allergy, Asthma, and Clinical Immunology, Department of Medicine, Mayo Clinic Arizona, Scottsdale, Ariz.
Danna R OrtizDivision of Allergy, Asthma, and Clinical Immunology, Department of Medicine, Mayo Clinic Arizona, Scottsdale, Ariz.
Aliviya R SchulzeDivision of Allergy, Asthma, and Clinical Immunology, Department of Medicine, Mayo Clinic Arizona, Scottsdale, Ariz.
Nicholas FritzSchool of Biological and Health Systems Engineering, Arizona State University, Tempe, Ariz.
Takao KobayashiDivision of Allergy, Asthma, and Clinical Immunology, Department of Medicine, Mayo Clinic Arizona, Scottsdale, Ariz.
Koji IijimaDivision of Allergy, Asthma, and Clinical Immunology, Department of Medicine, Mayo Clinic Arizona, Scottsdale, Ariz.
Andres J Klein-SzantoHistopathology Facility, Fox Chase Cancer Center, Philadelphia, Pa.
Masataka ShimonosonoDivision of Digestive and Liver Diseases, Department of Medicine and Herbert Irving Comprehensive Cancer Center, Columbia University Irving Medical Center, New York, NY.
Samuel FlashnerDivision of Digestive and Liver Diseases, Department of Medicine and Herbert Irving Comprehensive Cancer Center, Columbia University Irving Medical Center, New York, NY.
Masaki MorimotoDivision of Digestive and Liver Diseases, Department of Medicine and Herbert Irving Comprehensive Cancer Center, Columbia University Irving Medical Center, New York, NY.
Rish K PaiDivision of Pathology and Laboratory Medicine, Mayo Clinic Arizona, Scottsdale, Ariz.
Matthew A RankDivision of Allergy, Asthma, and Clinical Immunology, Department of Medicine, Mayo Clinic Arizona, Scottsdale, Ariz; Division of Allergy and Immunology, Phoenix Children's Hospital, Phoenix, Ariz.
Hiroshi NakagawaDivision of Digestive and Liver Diseases, Department of Medicine and Herbert Irving Comprehensive Cancer Center, Columbia University Irving Medical Center, New York, NY.
Hirohito KitaDivision of Allergy, Asthma, and Clinical Immunology, Department of Medicine, Mayo Clinic Arizona, Scottsdale, Ariz; Department of Immunology, Mayo Clinic, Rochester, and Mayo Clinic Arizona, Scottsdale, Ariz.
Benjamin L WrightDivision of Allergy, Asthma, and Clinical Immunology, Department of Medicine, Mayo Clinic Arizona, Scottsdale, Ariz; Division of Allergy and Immunology, Phoenix Children's Hospital, Phoenix, Ariz.
Alfred D DoyleDivision of Allergy, Asthma, and Clinical Immunology, Department of Medicine, Mayo Clinic Arizona, Scottsdale, Ariz. Electronic address: doyle.alfred@mayo.edu.
WinnMed · USColumbia University Irving Medical Center · USMayo Clinic · USArizona State University · USFox Chase Cancer Center · USMayo Clinic in Arizona · US

Funding

The Organoid and Cell Culture CoreP30DK132710 · NIDDK · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Robert F. Schwabe · 2022 to 2026
$7.2M
Mechanisms of IL-33 secretion in allergic diseasesR01AI128729 · NIAID · MAYO CLINIC ROCHESTER · PI Hirohito Kita, SCOTT M. O'GRADY · 2017 to 2026
$5.6M
Mechanisms of Allergen-induced Type 2 ImmunityR37AI071106 · NIAID · MAYO CLINIC ROCHESTER · PI Hirohito Kita · 2018 to 2026
$5.2M
Type 2 Innate Lymphoid Cells and AsthmaR01HL117823 · NHLBI · MAYO CLINIC ROCHESTER · PI KITA, HIROHITO · 2014 to 2021
$3.5M
Autophagy and esophageal tissue remodeling in EoER01DK114436 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI NAKAGAWA, HIROSHI · 2017 to 2024
$3.1M
Aldh2 and mitochondrial homeostasis in esophageal pathobiologyR01AA026297 · NIAAA · UNIVERSITY OF PENNSYLVANIA · PI Hiroshi Nakagawa · 2018 to 2026
$2.9M
Mechanisms of adverse gastrointestinal events during oral immunotherapyK23AI158813 · NIAID · MAYO CLINIC ARIZONA · PI Benjamin L. Wright · 2022 to 2026
$949k
NCI NIH HHS L30 CA264714NHLBI NIH HHS R01 HL117823NIAAA NIH HHS R01 AA026297NIAID NIH HHS K23 AI158813NIAID NIH HHS R01 AI128729NIAID NIH HHS R37 AI071106NIDDK NIH HHS P30 DK132710NIDDK NIH HHS R01 DK114436
6 · The paper itself

Abstract

backgroundEosinophilic esophagitis (EoE) is an increasingly common inflammatory condition of the esophagus; however, the underlying immunologic mechanisms remain poorly understood. The epithelium-derived cytokine IL-33 is associated with type 2 immune responses and elevated in esophageal biopsy specimens from patients with EoE.

objectiveWe hypothesized that overexpression of IL-33 by the esophageal epithelium would promote the immunopathology of EoE.

methodsWe evaluated the functional consequences of esophageal epithelial overexpression of a secreted and active form of IL-33 in a novel transgenic mouse, EoE33. EoE33 mice were analyzed for clinical and immunologic phenotypes. Esophageal contractility was assessed. Epithelial cytokine responses were analyzed in three-dimensional organoids. EoE33 phenotypes were further characterized in ST2

resultsEoE33 mice displayed ST2-dependent, EoE-like pathology and failed to thrive. Esophageal tissue remodeling and inflammation included basal zone hyperplasia, eosinophilia, mast cells, and T

conclusionsIL-33 overexpression by the esophageal epithelium generated immunopathology and clinical phenotypes resembling human EoE. IL-33 may play a pivotal role in the etiology of EoE by activating the IL-13 pathway. EoE33 mice are a robust experimental platform for mechanistic investigation and translational discovery.

Indexed as

Eosinophilic EsophagitisInterleukin-13Interleukin-33AnimalsDisease Models, AnimalEosinophilsEsophageal MucosaEsophagusHumansInterleukin-1 Receptor-Like 1 ProteinMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicIL13 protein, humanIL33 protein, humanIl33 protein, mouseInterleukin-13Interleukin-1 Receptor-Like 1 ProteinInterleukin-33eosinophileosinophilic esophagitisIL-33transgenetype 2 inflammation

Identifiers

PMID38310974
PMCPMC11070306
OpenAlexW4391513804

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.