Evidence map›Paper›PMID 39131849›Full record

ReviewGastro hep advances2022

Examining the Role of Type 2 Inflammation in Eosinophilic Esophagitis.

Mirna Chehade, Gary W Falk, Seema Aceves, Jason K Lee, Vinay Mehta, John Leung, Brad Shumel, Juby A Jacob-Nara, Yamo Deniz, Paul J Rowe and 2 more

Abstract readReview
In one paragraph

Review in Gastro hep advances, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
–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

12 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Trial
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Cow milk protein allergy mimics in infancy.World journal of clinical pediatrics · 2025
    Review
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  12. 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

12 authors.

Mirna ChehadeDeparment of Pediatrics and Medicine, Mount Sinai Center for Eosinophilic Disorders, Icahn School of Medicine at Mount Sinai, New York, New York.
Gary W FalkDivision of Gastroenterology, Department of Medicine, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania.
Seema AcevesDeparment of Pediatrics and Medicine, University of California, San Diego, California.
Jason K LeeDeparment of Clinical Immunology and Allergy and Internal Medicine, Toronto Allergy and Asthma Clinic, Toronto, Ontario, Canada.
Vinay MehtaAllergy, Asthma & Immunology Associates, P.C., Lincoln, Nebraska.
John LeungBoston Specialists, Boston, Massachusetts.
Brad ShumelRegeneron Pharmaceuticals, Inc, Tarrytown, New York.
Juby A Jacob-NaraSanofi, Bridgewater, New Jersey.
Yamo DenizRegeneron Pharmaceuticals, Inc, Tarrytown, New York.
Paul J RoweSanofi, Bridgewater, New Jersey.
Danen CunoosamySanofi, Cambridge, Massachusetts.
Angela KhodzhayevRegeneron Pharmaceuticals, Inc, Tarrytown, New York.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Eosinophilic esophagitis (EoE) is a chronic type 2 inflammatory disease characterized by an eosinophilic inflammatory infiltrate in the esophagus, leading to remodeling, stricture formation, and fibrosis. Triggered by food and aeroallergens, type 2 cytokines interleukin (IL)-4, IL-13, IL-5 produced by CD4+ T helper 2 cells (Th2), eosinophils, mast cells, basophils, and type 2 innate lymphoid cells alter the esophageal epithelial barrier and increase inflammatory cell tissue infiltration. Clustering analysis based on the expression of type 2 inflammatory genes demonstrated the diversity of EoE endotypes. Despite the availability of treatment options for patients with EoE, which include dietary restriction, proton pump inhibitors, swallowed topical steroids, and esophageal dilation, there are still no Food and Drug Administration-approved medications for this disease; as such, there are clear unmet medical needs for these patients. A number of novel biologic therapies currently in clinical trials represent a promising avenue for targeted therapeutic approaches in EoE. This review summarizes our current knowledge on the role of type 2 inflammatory cells and mediators in EoE disease pathogenesis, as well as the future treatment landscape targeting underlying inflammation in EoE.

Indexed as

EndotypesEosinophilic EsophagitisEosinophilsType 2 Inflammation

Identifiers

PMID39131849
PMCPMC11307682

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.