Eosinophilic Esophagitis

Complex MONDO:0005361 Pathograph 6 Show in embeddings browser Allergic Disease Chronic Inflammatory Disease Gastrointestinal Disease

Eosinophilic esophagitis (EoE) is a chronic, food- and aeroallergen-driven, type 2-mediated inflammatory disease of the esophagus that develops in genetically predisposed individuals with an impaired esophageal epithelial barrier. Converging genetic and functional data place the esophageal epithelium at the center of pathogenesis: epithelial-intrinsic susceptibility (e.g., loss of the protease inhibitor SPINK7 and risk variants in the esophagus-specific protease calpain 14) and environmental exposures (food allergens, detergents) drive release of epithelial alarmins (TSLP, IL-33), which activate ILC2 and Th2 cells, recruit eosinophils via eotaxin-3 (CCL26), and produce esophageal eosinophilia, tissue damage, and progressive subepithelial fibrosis. Clinically it presents with dysphagia and food impaction in adults and feeding difficulties, vomiting, and failure to thrive in children, and is diagnosed histologically by a peak count of at least 15 eosinophils per high-power field.

Ask OpenScientist

Ask a research question about Eosinophilic Esophagitis. OpenScientist will conduct autonomous deep research using the Disorder Mechanisms Knowledge Base and PubMed literature (typically 10-30 minutes).

Submitting...

Do not include personal health information in your question. Questions and results are cached in your browser's local storage.

6
Pathophys.
1
Histopath.
5
Phenotypes
1
Hypotheses
3
Gaps
6
Pathograph
5
Medical Actions
8
References
1
Hyp. Reports
◈

Mechanistic Hypotheses

1
Barrier-Antigen Type 2 Specificity Model
barrier_antigen_type2_specificity_model EMERGING
Esophageal epithelial barrier dysfunction increases exposure to food and aeroallergen antigens and triggers epithelial alarmin release. TSLP and IL-33 then polarize local ILC2/Th2 inflammation, IL-5/IL-13 responses, and CCL26-mediated eosinophil recruitment. The broad barrier-to-type-2 axis is well supported, but the patient-specific selection of food antigens remains an open mechanistic subproblem rather than a settled causal edge.
Pathograph links
Esophageal Epithelial Barrier Dysfunction -> Epithelial Alarmin Release Loss of barrier integrity and unleashed epithelial protease activity drives production of proinflammatory and proallergic alarmin cytokines, including thymic stromal lymphopoietin.
Environmental Detergent Exposure -> Esophageal Epithelial Barrier Dysfunction Detergent exposure decreases esophageal barrier integrity and promotes epithelial hyperplasia, providing an environmental route to barrier disruption.
Environmental Detergent Exposure -> Epithelial Alarmin Release Detergent exposure stimulates IL-33 production by esophageal epithelium, feeding the alarmin-driven type 2 response.
Epithelial Alarmin Release -> Type 2 Immune Activation Epithelial alarmins TSLP and IL-33 activate ILC2 and Th2 cells, polarizing the local immune response toward type 2 inflammation.
Type 2 Immune Activation -> Eosinophil Recruitment to Esophagus Type 2 cytokines (notably IL-5 and IL-13) drive eosinophil maturation and induce epithelial eotaxin-3 (CCL26) expression that recruits eosinophils to the esophageal mucosa.
Eosinophil Recruitment to Esophagus -> Esophageal Fibrosis and Remodeling Persistent eosinophil-driven inflammation and the type 2 cytokine milieu promote subepithelial fibrosis and esophageal remodeling.
Deep research
OpenScientist citations 35 citations 2026-06-04T01:08:19.144453
Show evidence (3 references)
PMID:19596009 SUPPORT Other
"Eosinophilic esophagitis is a recently recognized but expanding disorder characterized by antigen-driven eosinophil accumulation in the esophagus."
Establishes antigen-driven eosinophil accumulation as a central EoE mechanism.
PMID:19596009 SUPPORT Other
"The pathogenesis of eosinophilic esophagitis involves environmental and genetic factors, particularly food antigens and expression level of the eosinophil chemoattractant eotaxin-3, respectively."
Links food antigens and eotaxin-3/CCL26 biology within the mechanistic model.
PMID:29980278 SUPPORT Human Clinical
"Furthermore, genetic and functional data establish a primary role for impaired epithelial barrier function in disease susceptibility and pathoetiology."
Supports the epithelial barrier component of the model.
?

Discussions and Knowledge Gaps

3
Why do individual EoE patients react to different specific food antigens despite sharing a common esophageal epithelial barrier defect and type 2 inflammatory program?
KNOWLEDGE GAP OPEN gap_eoe_food_antigen_specificity
Attached to
pathophysiology#Esophageal Epithelial Barrier Dysfunction pathophysiology#Type 2 Immune Activation mechanistic_hypothesis#barrier_antigen_type2_specificity_model
A shared barrier defect and type 2 axis do not explain patient-specific antigen selectivity. The connecting mechanism likely involves pre-existing local IgE sensitization and Th2 memory to particular foods, but there is no clean mechanistic consensus, and it cannot currently be modeled as a single causal edge from barrier disruption to a defined antigen response.
Show evidence (1 reference)
PMID:30364207 SUPPORT Human Clinical
"However, several unmet needs are to be solved urgently, as finding a non-invasive disease-monitoring methods and biomarkers for routine practice, the development or new therapies, novel food allergy testing to detect triggering foods, drug, and doses required for initial therapy and safety..."
Review identifies better food allergy testing to detect triggering foods as an unmet need, supporting the antigen-specificity gap.
Is environmental detergent exposure a genuine upstream human causal trigger of EoE, or only a mechanistically plausible model-system association?
KNOWLEDGE GAP OPEN gap_eoe_detergent_human_causality
Attached to
pathophysiology#Environmental Detergent Exposure
Detergent (SDS) exposure impairs the esophageal barrier and induces IL-33 and eosinophilia in cell-culture and mouse models, but direct human causal evidence is lacking. Whether this represents a true initiating exposure in patients or an experimentally tractable proxy remains unresolved.
Which eosinophil-dependent versus eosinophil-independent effector mechanisms drive dysphagia and fibrostenotic symptoms in EoE?
KNOWLEDGE GAP OPEN gap_eoe_eosinophil_symptom_causality
Attached to
pathophysiology#Eosinophil Recruitment to Esophagus pathophysiology#Esophageal Fibrosis and Remodeling mechanistic_hypothesis#barrier_antigen_type2_specificity_model
Eosinophil recruitment is a defining histologic and diagnostic axis, but eosinophil depletion alone has not consistently translated into symptom improvement. The symptom-producing tissue effectors may include epithelial remodeling, mast cells, neuromuscular dysfunction, and fibrosis in addition to eosinophils.
Show evidence (1 reference)
PMID:29372536 SUPPORT Other
"Mepolizumab and reslizumab, two anti-IL-5 antibodies, were studied in children and adults with EoE and resulted in reduction of esophageal tissue and blood eosinophils, but no significant reduction in symptoms."
Review of biologic therapy trials supports a gap between eosinophil reduction and symptom improvement.
⚙

Pathophysiology

6
Esophageal Epithelial Barrier Dysfunction
Impaired esophageal epithelial barrier function is a primary and initiating abnormality in EoE. The main disease susceptibility loci encode epithelium-produced gene products, and profound loss of the serine protease inhibitor SPINK7 unleashes proteolytic activity that disrupts barrier integrity and triggers proinflammatory and proallergic cytokine release.
Barrier-Antigen Type 2 Specificity Model
Esophageal epithelial cell CL:0002252
SPINK7 hgnc:24643 CAPN14 hgnc:16664 DSG1 hgnc:3048
Downstream
Epithelial Alarmin Release Loss of barrier integrity and unleashed epithelial protease activity drives production of proinflammatory and proallergic alarmin cytokines, including thymic stromal lymphopoietin. Barrier-Antigen Type 2 Specificity Model
Show evidence (2 references)
PMID:29980278 SUPPORT Human Clinical
"Furthermore, genetic and functional data establish a primary role for impaired epithelial barrier function in disease susceptibility and pathoetiology."
Establishes impaired epithelial barrier function as a primary driver of EoE susceptibility and pathogenesis.
PMID:29980278 SUPPORT Human Clinical
"Profound lost expression of SPINK7 occurs in patients with EoE and is sufficient for unleashing increased proteolytic activity (including urokinase plasminogen activator), impaired barrier function, and production of large quantities of proinflammatory and proallergic cytokines, including thymic..."
SPINK7 loss is sufficient to impair barrier function and drive proallergic cytokine production, linking barrier dysfunction to downstream inflammation.
Environmental Detergent Exposure
Detergents such as sodium dodecyl sulfate (SDS), common in household products like dish soap and toothpaste, are proposed environmental triggers that decrease esophageal barrier integrity and stimulate IL-33 production. This node is supported by in vitro and mouse-model evidence and is best modeled as a mechanistically plausible environmental trigger rather than a confirmed human causal edge.
Barrier-Antigen Type 2 Specificity Model
Esophageal epithelial cell CL:0002252
IL33 hgnc:16028
Downstream
Esophageal Epithelial Barrier Dysfunction Detergent exposure decreases esophageal barrier integrity and promotes epithelial hyperplasia, providing an environmental route to barrier disruption. Barrier-Antigen Type 2 Specificity Model
Epithelial Alarmin Release Detergent exposure stimulates IL-33 production by esophageal epithelium, feeding the alarmin-driven type 2 response. Barrier-Antigen Type 2 Specificity Model
Show evidence (2 references)
PMID:35899466 SUPPORT In Vitro
"Exposure to SDS decreases esophageal barrier integrity, stimulates IL-33 production, and promotes epithelial hyperplasia and tissue eosinophilia."
Cell-culture and organoid experiments show SDS detergent exposure impairs the esophageal barrier and induces IL-33 and eosinophilia.
PMID:35899466 SUPPORT Model Organism
"Detergents may be a key environmental trigger in EoE pathogenesis."
Mouse-model data support detergent exposure as a candidate upstream environmental trigger of EoE.
Epithelial Alarmin Release
Barrier-disrupted esophageal epithelium releases alarmin cytokines, most notably thymic stromal lymphopoietin (TSLP) and IL-33, which initiate and amplify the downstream type 2 immune response. TSLP is encoded at a major EoE susceptibility locus and is produced by the esophageal epithelium.
Barrier-Antigen Type 2 Specificity Model
Esophageal epithelial cell CL:0002252
TSLP hgnc:30743 IL33 hgnc:16028
Positive regulation of inflammatory response GO:0050729 ↑ INCREASED
Downstream
Type 2 Immune Activation Epithelial alarmins TSLP and IL-33 activate ILC2 and Th2 cells, polarizing the local immune response toward type 2 inflammation. Barrier-Antigen Type 2 Specificity Model
Show evidence (1 reference)
PMID:29980278 SUPPORT Human Clinical
"In particular, the main EoE disease susceptibility loci at 2p23 and 5p22 encode for gene products that are produced by the esophageal epithelium: the intracellular protease calpain 14 and thymic stromal lymphopoietin, respectively."
TSLP is encoded at a major EoE susceptibility locus and produced by esophageal epithelium, supporting its role as an epithelial-derived driver.
Type 2 Immune Activation
Epithelial alarmins drive activation of group 2 innate lymphoid cells (ILC2) and T-helper 2 cells, generating a type 2 cytokine milieu (IL-4, IL-5, IL-13) that promotes IgE class switching, eosinophil maturation, and eotaxin-driven recruitment. Barrier dysfunction and T-helper 2 inflammation are considered the pathogenetically important factors in EoE.
Barrier-Antigen Type 2 Specificity Model
Group 2 innate lymphoid cell CL:0001069 T-helper 2 cell CL:0000546
IL13 hgnc:5973 IL5 hgnc:6016
Type 2 immune response GO:0042092 ↑ INCREASED Interleukin-13 production GO:0032616 ↑ INCREASED
Downstream
Eosinophil Recruitment to Esophagus Type 2 cytokines (notably IL-5 and IL-13) drive eosinophil maturation and induce epithelial eotaxin-3 (CCL26) expression that recruits eosinophils to the esophageal mucosa. Barrier-Antigen Type 2 Specificity Model
Show evidence (2 references)
PMID:30364207 SUPPORT Human Clinical
"Barrier dysfunction and T-helper 2 inflammation is considered to be pathogenetically important factors."
Identifies T-helper 2 inflammation, alongside barrier dysfunction, as a core pathogenetic factor in EoE.
PMID:19596009 SUPPORT Other
"Analyses of gene expression signatures and animal models have indicated the importance of adaptive T-cell immunity that involves interleukin-5 and interleukin-13-induced esophageal epithelial cell responses."
Supports IL-5/IL-13-associated adaptive immune activation and epithelial response in EoE.
Eosinophil Recruitment to Esophagus
Type 2 cytokines induce epithelial expression of eotaxin-3 (CCL26), the dominant chemokine recruiting eosinophils into the esophageal mucosa. The resulting esophageal eosinophilia (diagnostic threshold of at least 15 eosinophils per high-power field) and degranulation cause tissue damage.
Barrier-Antigen Type 2 Specificity Model
Eosinophil CL:0000771
CCL26 hgnc:10625
Eosinophil chemotaxis GO:0048245 ↑ INCREASED
Downstream
Esophageal Fibrosis and Remodeling Persistent eosinophil-driven inflammation and the type 2 cytokine milieu promote subepithelial fibrosis and esophageal remodeling. Barrier-Antigen Type 2 Specificity Model
Show evidence (2 references)
PMID:30364207 SUPPORT Human Clinical
"The diagnostic criteria for EoE has evolved but mainly requires symptoms of esophageal dysfunction with histologic evidence of a peak value of at least 15 eosinophils per high-power field."
Defines the histologic hallmark of esophageal eosinophilia (>=15 eos/hpf) central to this node.
PMID:19596009 SUPPORT Other
"The pathogenesis of eosinophilic esophagitis involves environmental and genetic factors, particularly food antigens and expression level of the eosinophil chemoattractant eotaxin-3, respectively."
Supports food-antigen-linked eotaxin-3/CCL26 activity as part of eosinophil recruitment biology.
Esophageal Fibrosis and Remodeling
Chronic type 2 inflammation drives subepithelial fibrosis, lamina propria remodeling, and stricture formation. This fibrostenotic remodeling underlies the dysphagia and food impaction that characterize long-standing, inadequately treated disease.
Extracellular matrix organization GO:0030198 ↑ INCREASED Fibroblast activation GO:0072537 ↑ INCREASED
Show evidence (2 references)
PMID:30364207 SUPPORT Human Clinical
"Endoscopic dilation is used for patients with severe dysphagia/food impaction with inadequate response to anti-inflammatory treatment."
The need for mechanical dilation in refractory disease reflects fibrostenotic remodeling and stricture, the clinical endpoint of this node.
PMID:26857345 SUPPORT Human Clinical
"We developed a histology scoring system for esophageal biopsies that evaluates eight features: eosinophil density, basal zone hyperplasia, eosinophil abscesses, eosinophil surface layering, dilated intercellular spaces (DIS), surface epithelial alteration, dyskeratotic epithelial cells, and..."
Direct human biopsy evidence includes lamina propria fibrosis and epithelial remodeling among EoE histologic features.
✶

Histopathology

1
EoE histologic remodeling score features
EoE biopsies are assessed beyond peak eosinophil counts using a composite pattern that includes eosinophil density, basal zone hyperplasia, eosinophil abscesses, surface layering, dilated intercellular spaces, surface epithelial alteration, dyskeratotic epithelial cells, and lamina propria fibrosis.
Show evidence (1 reference)
PMID:26857345 SUPPORT Human Clinical
"We developed a histology scoring system for esophageal biopsies that evaluates eight features: eosinophil density, basal zone hyperplasia, eosinophil abscesses, eosinophil surface layering, dilated intercellular spaces (DIS), surface epithelial alteration, dyskeratotic epithelial cells, and..."
Validated EoE histology score supports the composite epithelial and fibrotic remodeling pattern.
⬡

Pathograph

Use the checkboxes to hide or show graph categories. Hover nodes for evidence and cross-linked metadata.
Pathograph: causal mechanism network for Eosinophilic Esophagitis Interactive directed graph showing how pathophysiology mechanisms, phenotypes, genetic factors and variants, experimental models, environmental triggers, and treatments relate through causal and linked edges.
●

Phenotypes

5
Digestive 3
Dysphagia Dysphagia HP:0002015
Difficulty swallowing, particularly for solids, is the dominant presenting symptom in adolescents and adults.
Show evidence (1 reference)
PMID:30364207 SUPPORT Human Clinical
"Eosinophilic esophagitis (EoE) was first described in the 1990s, showing an increasing incidence and prevalence since then, being the leading cause of food impaction and the major cause of dysphagia."
EoE is identified as a major cause of dysphagia.
Esophageal stricture Esophageal stricture HP:0002043
Fibrostenotic remodeling produces fixed esophageal narrowing in long-standing disease.
Show evidence (1 reference)
PMID:30364207 SUPPORT Human Clinical
"Endoscopic dilation is used for patients with severe dysphagia/food impaction with inadequate response to anti-inflammatory treatment."
The clinical use of endoscopic dilation reflects fixed strictures from fibrostenotic remodeling.
Feeding difficulties Feeding difficulties HP:0011968
In infants and young children, EoE more often presents with feeding difficulties, vomiting, and failure to thrive than with classic dysphagia.
Show evidence (1 reference)
PMID:30364207 SUPPORT Human Clinical
"There are different patterns of clinical presentation varying with age and can be masked by adaptation habits."
Age-dependent presentation underlies the feeding-related symptoms seen in younger children.
Other 2
Esophageal food impaction Esophageal food impaction HP:0031984
Acute bolus impaction is a common emergency presentation and the leading structural consequence of fibrostenotic disease.
Show evidence (1 reference)
PMID:30364207 SUPPORT Human Clinical
"being the leading cause of food impaction and the major cause of dysphagia."
EoE is the leading cause of food impaction.
Esophageal eosinophilia Eosinophilic infiltration of the esophagus HP:0410151
Histologic peak count of at least 15 eosinophils per high-power field on esophageal biopsy is the diagnostic hallmark.
Show evidence (1 reference)
PMID:30364207 SUPPORT Human Clinical
"mainly requires symptoms of esophageal dysfunction with histologic evidence of a peak value of at least 15 eosinophils per high-power field."
Esophageal eosinophilia at >=15 eos/hpf is the defining histologic feature of EoE.
💊

Medical Actions

5
Proton Pump Inhibitor Therapy
Action: proton pump inhibitor agent therapy MAXO:0000272
Agent: omeprazole CHEBI:7772
Proton pump inhibitors (e.g., omeprazole) are a first-line pharmacologic option that induces histologic and symptomatic remission in a substantial subset of patients with EoE.
Show evidence (1 reference)
PMID:30364207 SUPPORT Human Clinical
"Treatment of EoE can be started either by drugs (PPIs and topical corticosteroids) or elimination diets."
PPIs are an established first-line drug treatment for EoE.
Swallowed Topical Corticosteroid Therapy
Action: Pharmacotherapy NCIT:C15986
Agent: budesonide CHEBI:3207
Swallowed topical corticosteroids (e.g., budesonide or fluticasone formulations) deliver anti-inflammatory therapy to the esophageal mucosa and are a first-line option to induce histologic remission.
Show evidence (1 reference)
PMID:30364207 SUPPORT Human Clinical
"Treatment of EoE can be started either by drugs (PPIs and topical corticosteroids) or elimination diets."
Topical corticosteroids are an established first-line anti-inflammatory drug treatment for EoE.
Dietary Elimination Therapy
Action: dietary intervention MAXO:0000088
Empiric food-elimination diets (including step-up multistage and six-food elimination approaches) remove triggering antigens and can induce histologic remission, identifying causative foods through reintroduction.
Show evidence (1 reference)
PMID:30364207 SUPPORT Human Clinical
"The multistage step-up elimination diet management approach of EoE is promising."
Step-up elimination diet is an established non-pharmacologic management strategy for EoE.
Dupilumab
Action: Pharmacotherapy NCIT:C15986
Agent: dupilumab NCIT:C162455
Dupilumab is a monoclonal antibody targeting the IL-4 receptor alpha subunit, blocking IL-4 and IL-13 signaling at the core of the type 2 inflammatory axis; it is approved for EoE.
Show evidence (1 reference)
PMID:36546624 SUPPORT Human Clinical
"Among patients with eosinophilic esophagitis, subcutaneous dupilumab administered weekly improved histologic outcomes and alleviated symptoms of the disease."
The pivotal phase 3 LIBERTY EoE TREET trial (NCT03633617) demonstrated that IL-4Rα blockade with dupilumab achieves histologic remission and symptom improvement in EoE, the efficacy basis for its FDA approval (May 2022).
Endoscopic Esophageal Dilation
Action: esophageal dilation Ontology label: Esophageal Dilation NCIT:C70908
Endoscopic dilation mechanically relieves fibrostenotic strictures and is reserved for patients with severe dysphagia or food impaction not adequately controlled by anti-inflammatory therapy.
Show evidence (1 reference)
PMID:30364207 SUPPORT Human Clinical
"Endoscopic dilation is used for patients with severe dysphagia/food impaction with inadequate response to anti-inflammatory treatment."
Defines the indication for endoscopic dilation in refractory fibrostenotic EoE.
{ }

Source YAML

click to show 
name: Eosinophilic Esophagitis
creation_date: '2026-06-03T00:00:00Z'
category: Complex
parents:
- Allergic Disease
- Chronic Inflammatory Disease
- Gastrointestinal Disease
description: >-
  Eosinophilic esophagitis (EoE) is a chronic, food- and aeroallergen-driven,
  type 2-mediated inflammatory disease of the esophagus that develops in
  genetically predisposed individuals with an impaired esophageal epithelial
  barrier. Converging genetic and functional data place the esophageal
  epithelium at the center of pathogenesis: epithelial-intrinsic susceptibility
  (e.g., loss of the protease inhibitor SPINK7 and risk variants in the
  esophagus-specific protease calpain 14) and environmental exposures
  (food allergens, detergents) drive release of epithelial alarmins
  (TSLP, IL-33), which activate ILC2 and Th2 cells, recruit eosinophils via
  eotaxin-3 (CCL26), and produce esophageal eosinophilia, tissue damage, and
  progressive subepithelial fibrosis. Clinically it presents with dysphagia
  and food impaction in adults and feeding difficulties, vomiting, and failure
  to thrive in children, and is diagnosed histologically by a peak count of at
  least 15 eosinophils per high-power field.
synonyms:
- EoE
- allergic esophagitis
prevalence:
- population: Global
  notes: >-
    EoE has shown an increasing incidence and prevalence since its description
    in the 1990s and is the leading cause of food impaction and a major cause of
    dysphagia. It affects both children and adults, with a male predominance,
    and is frequently associated with atopic disease and IgE-mediated food
    allergies.
  evidence:
  - reference: PMID:30364207
    reference_title: "Eosinophilic Esophagitis: Review and Update."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "Eosinophilic esophagitis (EoE) was first described in the 1990s, showing an increasing incidence and prevalence since then, being the leading cause of food impaction and the major cause of dysphagia."
    explanation: Review establishes EoE epidemiology as an increasingly prevalent disorder and the leading cause of food impaction.
mechanistic_hypotheses:
- hypothesis_group_id: barrier_antigen_type2_specificity_model
  hypothesis_label: Barrier-Antigen Type 2 Specificity Model
  status: EMERGING
  description: >-
    Esophageal epithelial barrier dysfunction increases exposure to food and
    aeroallergen antigens and triggers epithelial alarmin release. TSLP and
    IL-33 then polarize local ILC2/Th2 inflammation, IL-5/IL-13 responses, and
    CCL26-mediated eosinophil recruitment. The broad barrier-to-type-2 axis is
    well supported, but the patient-specific selection of food antigens remains
    an open mechanistic subproblem rather than a settled causal edge.
  evidence:
  - reference: PMID:19596009
    reference_title: "Biology and treatment of eosinophilic esophagitis."
    supports: SUPPORT
    evidence_source: OTHER
    snippet: "Eosinophilic esophagitis is a recently recognized but expanding disorder characterized by antigen-driven eosinophil accumulation in the esophagus."
    explanation: Establishes antigen-driven eosinophil accumulation as a central EoE mechanism.
  - reference: PMID:19596009
    reference_title: "Biology and treatment of eosinophilic esophagitis."
    supports: SUPPORT
    evidence_source: OTHER
    snippet: "The pathogenesis of eosinophilic esophagitis involves environmental and genetic factors, particularly food antigens and expression level of the eosinophil chemoattractant eotaxin-3, respectively."
    explanation: Links food antigens and eotaxin-3/CCL26 biology within the mechanistic model.
  - reference: PMID:29980278
    reference_title: "Epithelial origin of eosinophilic esophagitis."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "Furthermore, genetic and functional data establish a primary role for impaired epithelial barrier function in disease susceptibility and pathoetiology."
    explanation: Supports the epithelial barrier component of the model.
pathophysiology:
- name: Esophageal Epithelial Barrier Dysfunction
  conforms_to: "epithelial_barrier_dysfunction#Epithelial Barrier Insult and Junctional Disruption"
  description: >-
    Impaired esophageal epithelial barrier function is a primary and initiating
    abnormality in EoE. The main disease susceptibility loci encode
    epithelium-produced gene products, and profound loss of the serine protease
    inhibitor SPINK7 unleashes proteolytic activity that disrupts barrier
    integrity and triggers proinflammatory and proallergic cytokine release.
  genes:
  - preferred_term: SPINK7
    term:
      id: hgnc:24643
      label: SPINK7
  - preferred_term: CAPN14
    term:
      id: hgnc:16664
      label: CAPN14
  - preferred_term: DSG1
    term:
      id: hgnc:3048
      label: DSG1
  cell_types:
  - preferred_term: Esophageal epithelial cell
    term:
      id: CL:0002252
      label: epithelial cell of esophagus
  downstream:
  - target: Epithelial Alarmin Release
    description: >-
      Loss of barrier integrity and unleashed epithelial protease activity
      drives production of proinflammatory and proallergic alarmin cytokines,
      including thymic stromal lymphopoietin.
    hypothesis_groups:
    - barrier_antigen_type2_specificity_model
  evidence:
  - reference: PMID:29980278
    reference_title: "Epithelial origin of eosinophilic esophagitis."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "Furthermore, genetic and functional data establish a primary role for impaired epithelial barrier function in disease susceptibility and pathoetiology."
    explanation: Establishes impaired epithelial barrier function as a primary driver of EoE susceptibility and pathogenesis.
  - reference: PMID:29980278
    reference_title: "Epithelial origin of eosinophilic esophagitis."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "Profound lost expression of SPINK7 occurs in patients with EoE and is sufficient for unleashing increased proteolytic activity (including urokinase plasminogen activator), impaired barrier function, and production of large quantities of proinflammatory and proallergic cytokines, including thymic stromal lymphopoietin."
    explanation: SPINK7 loss is sufficient to impair barrier function and drive proallergic cytokine production, linking barrier dysfunction to downstream inflammation.
- name: Environmental Detergent Exposure
  description: >-
    Detergents such as sodium dodecyl sulfate (SDS), common in household products
    like dish soap and toothpaste, are proposed environmental triggers that
    decrease esophageal barrier integrity and stimulate IL-33 production. This
    node is supported by in vitro and mouse-model evidence and is best modeled
    as a mechanistically plausible environmental trigger rather than a confirmed
    human causal edge.
  genes:
  - preferred_term: IL33
    term:
      id: hgnc:16028
      label: IL33
  cell_types:
  - preferred_term: Esophageal epithelial cell
    term:
      id: CL:0002252
      label: epithelial cell of esophagus
  downstream:
  - target: Esophageal Epithelial Barrier Dysfunction
    description: >-
      Detergent exposure decreases esophageal barrier integrity and promotes
      epithelial hyperplasia, providing an environmental route to barrier
      disruption.
    hypothesis_groups:
    - barrier_antigen_type2_specificity_model
  - target: Epithelial Alarmin Release
    description: >-
      Detergent exposure stimulates IL-33 production by esophageal epithelium,
      feeding the alarmin-driven type 2 response.
    hypothesis_groups:
    - barrier_antigen_type2_specificity_model
  evidence:
  - reference: PMID:35899466
    reference_title: "Detergent exposure induces epithelial barrier dysfunction and eosinophilic inflammation in the esophagus."
    supports: SUPPORT
    evidence_source: IN_VITRO
    snippet: "Exposure to SDS decreases esophageal barrier integrity, stimulates IL-33 production, and promotes epithelial hyperplasia and tissue eosinophilia."
    explanation: Cell-culture and organoid experiments show SDS detergent exposure impairs the esophageal barrier and induces IL-33 and eosinophilia.
  - reference: PMID:35899466
    reference_title: "Detergent exposure induces epithelial barrier dysfunction and eosinophilic inflammation in the esophagus."
    supports: SUPPORT
    evidence_source: MODEL_ORGANISM
    snippet: "Detergents may be a key environmental trigger in EoE pathogenesis."
    explanation: Mouse-model data support detergent exposure as a candidate upstream environmental trigger of EoE.
- name: Epithelial Alarmin Release
  description: >-
    Barrier-disrupted esophageal epithelium releases alarmin cytokines, most
    notably thymic stromal lymphopoietin (TSLP) and IL-33, which initiate and
    amplify the downstream type 2 immune response. TSLP is encoded at a major
    EoE susceptibility locus and is produced by the esophageal epithelium.
  genes:
  - preferred_term: TSLP
    term:
      id: hgnc:30743
      label: TSLP
  - preferred_term: IL33
    term:
      id: hgnc:16028
      label: IL33
  biological_processes:
  - preferred_term: Positive regulation of inflammatory response
    term:
      id: GO:0050729
      label: positive regulation of inflammatory response
    modifier: INCREASED
  cell_types:
  - preferred_term: Esophageal epithelial cell
    term:
      id: CL:0002252
      label: epithelial cell of esophagus
  downstream:
  - target: Type 2 Immune Activation
    description: >-
      Epithelial alarmins TSLP and IL-33 activate ILC2 and Th2 cells, polarizing
      the local immune response toward type 2 inflammation.
    hypothesis_groups:
    - barrier_antigen_type2_specificity_model
  evidence:
  - reference: PMID:29980278
    reference_title: "Epithelial origin of eosinophilic esophagitis."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "In particular, the main EoE disease susceptibility loci at 2p23 and 5p22 encode for gene products that are produced by the esophageal epithelium: the intracellular protease calpain 14 and thymic stromal lymphopoietin, respectively."
    explanation: TSLP is encoded at a major EoE susceptibility locus and produced by esophageal epithelium, supporting its role as an epithelial-derived driver.
- name: Type 2 Immune Activation
  description: >-
    Epithelial alarmins drive activation of group 2 innate lymphoid cells (ILC2)
    and T-helper 2 cells, generating a type 2 cytokine milieu (IL-4, IL-5,
    IL-13) that promotes IgE class switching, eosinophil maturation, and
    eotaxin-driven recruitment. Barrier dysfunction and T-helper 2 inflammation
    are considered the pathogenetically important factors in EoE.
  genes:
  - preferred_term: IL13
    term:
      id: hgnc:5973
      label: IL13
  - preferred_term: IL5
    term:
      id: hgnc:6016
      label: IL5
  biological_processes:
  - preferred_term: Type 2 immune response
    term:
      id: GO:0042092
      label: type 2 immune response
    modifier: INCREASED
  - preferred_term: Interleukin-13 production
    term:
      id: GO:0032616
      label: interleukin-13 production
    modifier: INCREASED
  cell_types:
  - preferred_term: Group 2 innate lymphoid cell
    term:
      id: CL:0001069
      label: group 2 innate lymphoid cell
  - preferred_term: T-helper 2 cell
    term:
      id: CL:0000546
      label: T-helper 2 cell
  downstream:
  - target: Eosinophil Recruitment to Esophagus
    description: >-
      Type 2 cytokines (notably IL-5 and IL-13) drive eosinophil maturation and
      induce epithelial eotaxin-3 (CCL26) expression that recruits eosinophils
      to the esophageal mucosa.
    hypothesis_groups:
    - barrier_antigen_type2_specificity_model
  evidence:
  - reference: PMID:30364207
    reference_title: "Eosinophilic Esophagitis: Review and Update."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "Barrier dysfunction and T-helper 2 inflammation is considered to be pathogenetically important factors."
    explanation: Identifies T-helper 2 inflammation, alongside barrier dysfunction, as a core pathogenetic factor in EoE.
  - reference: PMID:19596009
    reference_title: "Biology and treatment of eosinophilic esophagitis."
    supports: SUPPORT
    evidence_source: OTHER
    snippet: "Analyses of gene expression signatures and animal models have indicated the importance of adaptive T-cell immunity that involves interleukin-5 and interleukin-13-induced esophageal epithelial cell responses."
    explanation: Supports IL-5/IL-13-associated adaptive immune activation and epithelial response in EoE.
- name: Eosinophil Recruitment to Esophagus
  description: >-
    Type 2 cytokines induce epithelial expression of eotaxin-3 (CCL26), the
    dominant chemokine recruiting eosinophils into the esophageal mucosa. The
    resulting esophageal eosinophilia (diagnostic threshold of at least 15
    eosinophils per high-power field) and degranulation cause tissue damage.
  genes:
  - preferred_term: CCL26
    term:
      id: hgnc:10625
      label: CCL26
  biological_processes:
  - preferred_term: Eosinophil chemotaxis
    term:
      id: GO:0048245
      label: eosinophil chemotaxis
    modifier: INCREASED
  cell_types:
  - preferred_term: Eosinophil
    term:
      id: CL:0000771
      label: eosinophil
  downstream:
  - target: Esophageal Fibrosis and Remodeling
    description: >-
      Persistent eosinophil-driven inflammation and the type 2 cytokine milieu
      promote subepithelial fibrosis and esophageal remodeling.
    hypothesis_groups:
    - barrier_antigen_type2_specificity_model
  evidence:
  - reference: PMID:30364207
    reference_title: "Eosinophilic Esophagitis: Review and Update."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "The diagnostic criteria for EoE has evolved but mainly requires symptoms of esophageal dysfunction with histologic evidence of a peak value of at least 15 eosinophils per high-power field."
    explanation: Defines the histologic hallmark of esophageal eosinophilia (>=15 eos/hpf) central to this node.
  - reference: PMID:19596009
    reference_title: "Biology and treatment of eosinophilic esophagitis."
    supports: SUPPORT
    evidence_source: OTHER
    snippet: "The pathogenesis of eosinophilic esophagitis involves environmental and genetic factors, particularly food antigens and expression level of the eosinophil chemoattractant eotaxin-3, respectively."
    explanation: Supports food-antigen-linked eotaxin-3/CCL26 activity as part of eosinophil recruitment biology.
- name: Esophageal Fibrosis and Remodeling
  description: >-
    Chronic type 2 inflammation drives subepithelial fibrosis, lamina propria
    remodeling, and stricture formation. This fibrostenotic remodeling underlies
    the dysphagia and food impaction that characterize long-standing,
    inadequately treated disease.
  biological_processes:
  - preferred_term: Extracellular matrix organization
    term:
      id: GO:0030198
      label: extracellular matrix organization
    modifier: INCREASED
  - preferred_term: Fibroblast activation
    term:
      id: GO:0072537
      label: fibroblast activation
    modifier: INCREASED
  evidence:
  - reference: PMID:30364207
    reference_title: "Eosinophilic Esophagitis: Review and Update."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "Endoscopic dilation is used for patients with severe dysphagia/food impaction with inadequate response to anti-inflammatory treatment."
    explanation: The need for mechanical dilation in refractory disease reflects fibrostenotic remodeling and stricture, the clinical endpoint of this node.
  - reference: PMID:26857345
    reference_title: "Newly developed and validated eosinophilic esophagitis histology scoring system and evidence that it outperforms peak eosinophil count for disease diagnosis and monitoring."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "We developed a histology scoring system for esophageal biopsies that evaluates eight features: eosinophil density, basal zone hyperplasia, eosinophil abscesses, eosinophil surface layering, dilated intercellular spaces (DIS), surface epithelial alteration, dyskeratotic epithelial cells, and lamina propria fibrosis."
    explanation: Direct human biopsy evidence includes lamina propria fibrosis and epithelial remodeling among EoE histologic features.
histopathology:
- name: EoE histologic remodeling score features
  description: >-
    EoE biopsies are assessed beyond peak eosinophil counts using a composite
    pattern that includes eosinophil density, basal zone hyperplasia,
    eosinophil abscesses, surface layering, dilated intercellular spaces,
    surface epithelial alteration, dyskeratotic epithelial cells, and lamina
    propria fibrosis.
  evidence:
  - reference: PMID:26857345
    reference_title: "Newly developed and validated eosinophilic esophagitis histology scoring system and evidence that it outperforms peak eosinophil count for disease diagnosis and monitoring."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "We developed a histology scoring system for esophageal biopsies that evaluates eight features: eosinophil density, basal zone hyperplasia, eosinophil abscesses, eosinophil surface layering, dilated intercellular spaces (DIS), surface epithelial alteration, dyskeratotic epithelial cells, and lamina propria fibrosis."
    explanation: Validated EoE histology score supports the composite epithelial and fibrotic remodeling pattern.
phenotypes:
- name: Dysphagia
  category: Gastrointestinal
  diagnostic: true
  notes: Difficulty swallowing, particularly for solids, is the dominant presenting symptom in adolescents and adults.
  phenotype_term:
    preferred_term: Dysphagia
    term:
      id: HP:0002015
      label: Dysphagia
  evidence:
  - reference: PMID:30364207
    reference_title: "Eosinophilic Esophagitis: Review and Update."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "Eosinophilic esophagitis (EoE) was first described in the 1990s, showing an increasing incidence and prevalence since then, being the leading cause of food impaction and the major cause of dysphagia."
    explanation: EoE is identified as a major cause of dysphagia.
- name: Esophageal food impaction
  category: Gastrointestinal
  notes: Acute bolus impaction is a common emergency presentation and the leading structural consequence of fibrostenotic disease.
  phenotype_term:
    preferred_term: Esophageal food impaction
    term:
      id: HP:0031984
      label: Esophageal food impaction
  evidence:
  - reference: PMID:30364207
    reference_title: "Eosinophilic Esophagitis: Review and Update."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "being the leading cause of food impaction and the major cause of dysphagia."
    explanation: EoE is the leading cause of food impaction.
- name: Esophageal eosinophilia
  category: Histopathological
  diagnostic: true
  notes: Histologic peak count of at least 15 eosinophils per high-power field on esophageal biopsy is the diagnostic hallmark.
  phenotype_term:
    preferred_term: Esophageal eosinophilia (>=15 eosinophils per high-power field)
    term:
      id: HP:0410151
      label: Eosinophilic infiltration of the esophagus
  evidence:
  - reference: PMID:30364207
    reference_title: "Eosinophilic Esophagitis: Review and Update."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "mainly requires symptoms of esophageal dysfunction with histologic evidence of a peak value of at least 15 eosinophils per high-power field."
    explanation: Esophageal eosinophilia at >=15 eos/hpf is the defining histologic feature of EoE.
- name: Esophageal stricture
  category: Gastrointestinal
  notes: Fibrostenotic remodeling produces fixed esophageal narrowing in long-standing disease.
  phenotype_term:
    preferred_term: Esophageal stricture
    term:
      id: HP:0002043
      label: Esophageal stricture
  evidence:
  - reference: PMID:30364207
    reference_title: "Eosinophilic Esophagitis: Review and Update."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "Endoscopic dilation is used for patients with severe dysphagia/food impaction with inadequate response to anti-inflammatory treatment."
    explanation: The clinical use of endoscopic dilation reflects fixed strictures from fibrostenotic remodeling.
- name: Feeding difficulties
  category: Gastrointestinal
  notes: In infants and young children, EoE more often presents with feeding difficulties, vomiting, and failure to thrive than with classic dysphagia.
  phenotype_term:
    preferred_term: Feeding difficulties
    term:
      id: HP:0011968
      label: Feeding difficulties
  evidence:
  - reference: PMID:30364207
    reference_title: "Eosinophilic Esophagitis: Review and Update."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "There are different patterns of clinical presentation varying with age and can be masked by adaptation habits."
    explanation: Age-dependent presentation underlies the feeding-related symptoms seen in younger children.
treatments:
- name: Proton Pump Inhibitor Therapy
  description: >-
    Proton pump inhibitors (e.g., omeprazole) are a first-line pharmacologic
    option that induces histologic and symptomatic remission in a substantial
    subset of patients with EoE.
  therapeutic_modality: SMALL_MOLECULE
  treatment_term:
    preferred_term: proton pump inhibitor agent therapy
    term:
      id: MAXO:0000272
      label: proton pump inhibitor agent therapy
    therapeutic_agent:
    - preferred_term: omeprazole
      term:
        id: CHEBI:7772
        label: omeprazole
  evidence:
  - reference: PMID:30364207
    reference_title: "Eosinophilic Esophagitis: Review and Update."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "Treatment of EoE can be started either by drugs (PPIs and topical corticosteroids) or elimination diets."
    explanation: PPIs are an established first-line drug treatment for EoE.
- name: Swallowed Topical Corticosteroid Therapy
  description: >-
    Swallowed topical corticosteroids (e.g., budesonide or fluticasone
    formulations) deliver anti-inflammatory therapy to the esophageal mucosa and
    are a first-line option to induce histologic remission.
  therapeutic_modality: SMALL_MOLECULE
  treatment_term:
    preferred_term: Pharmacotherapy
    term:
      id: NCIT:C15986
      label: Pharmacotherapy
    therapeutic_agent:
    - preferred_term: budesonide
      term:
        id: CHEBI:3207
        label: budesonide
  evidence:
  - reference: PMID:30364207
    reference_title: "Eosinophilic Esophagitis: Review and Update."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "Treatment of EoE can be started either by drugs (PPIs and topical corticosteroids) or elimination diets."
    explanation: Topical corticosteroids are an established first-line anti-inflammatory drug treatment for EoE.
- name: Dietary Elimination Therapy
  description: >-
    Empiric food-elimination diets (including step-up multistage and six-food
    elimination approaches) remove triggering antigens and can induce histologic
    remission, identifying causative foods through reintroduction.
  therapeutic_modality: BEHAVIORAL
  treatment_term:
    preferred_term: dietary intervention
    term:
      id: MAXO:0000088
      label: dietary intervention
  evidence:
  - reference: PMID:30364207
    reference_title: "Eosinophilic Esophagitis: Review and Update."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "The multistage step-up elimination diet management approach of EoE is promising."
    explanation: Step-up elimination diet is an established non-pharmacologic management strategy for EoE.
- name: Dupilumab
  description: >-
    Dupilumab is a monoclonal antibody targeting the IL-4 receptor alpha subunit,
    blocking IL-4 and IL-13 signaling at the core of the type 2 inflammatory
    axis; it is approved for EoE.
  therapeutic_modality: MONOCLONAL_ANTIBODY
  treatment_term:
    preferred_term: Pharmacotherapy
    term:
      id: NCIT:C15986
      label: Pharmacotherapy
    therapeutic_agent:
    - preferred_term: dupilumab
      term:
        id: NCIT:C162455
        label: Dupilumab
  evidence:
  - reference: PMID:36546624
    reference_title: "Dupilumab in Adults and Adolescents with Eosinophilic Esophagitis."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "Among patients with eosinophilic esophagitis, subcutaneous dupilumab administered weekly improved histologic outcomes and alleviated symptoms of the disease."
    explanation: The pivotal phase 3 LIBERTY EoE TREET trial (NCT03633617) demonstrated that IL-4Rα blockade with dupilumab achieves histologic remission and symptom improvement in EoE, the efficacy basis for its FDA approval (May 2022).
- name: Endoscopic Esophageal Dilation
  description: >-
    Endoscopic dilation mechanically relieves fibrostenotic strictures and is
    reserved for patients with severe dysphagia or food impaction not adequately
    controlled by anti-inflammatory therapy.
  therapeutic_modality: DEVICE
  treatment_term:
    preferred_term: esophageal dilation
    term:
      id: NCIT:C70908
      label: Esophageal Dilation
  evidence:
  - reference: PMID:30364207
    reference_title: "Eosinophilic Esophagitis: Review and Update."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "Endoscopic dilation is used for patients with severe dysphagia/food impaction with inadequate response to anti-inflammatory treatment."
    explanation: Defines the indication for endoscopic dilation in refractory fibrostenotic EoE.
discussions:
- discussion_id: gap_eoe_food_antigen_specificity
  prompt: >-
    Why do individual EoE patients react to different specific food antigens
    despite sharing a common esophageal epithelial barrier defect and type 2
    inflammatory program?
  kind: KNOWLEDGE_GAP
  status: OPEN
  attaches_to:
  - pathophysiology#Esophageal Epithelial Barrier Dysfunction
  - pathophysiology#Type 2 Immune Activation
  - mechanistic_hypothesis#barrier_antigen_type2_specificity_model
  rationale: >-
    A shared barrier defect and type 2 axis do not explain patient-specific
    antigen selectivity. The connecting mechanism likely involves pre-existing
    local IgE sensitization and Th2 memory to particular foods, but there is no
    clean mechanistic consensus, and it cannot currently be modeled as a single
    causal edge from barrier disruption to a defined antigen response.
  evidence:
  - reference: PMID:30364207
    reference_title: "Eosinophilic Esophagitis: Review and Update."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "However, several unmet needs are to be solved urgently, as finding a non-invasive disease-monitoring methods and biomarkers for routine practice, the development or new therapies, novel food allergy testing to detect triggering foods, drug, and doses required for initial therapy and safety issues with long-term maintenance therapy, amongst others."
    explanation: Review identifies better food allergy testing to detect triggering foods as an unmet need, supporting the antigen-specificity gap.
- discussion_id: gap_eoe_detergent_human_causality
  prompt: >-
    Is environmental detergent exposure a genuine upstream human causal trigger
    of EoE, or only a mechanistically plausible model-system association?
  kind: KNOWLEDGE_GAP
  status: OPEN
  attaches_to:
  - pathophysiology#Environmental Detergent Exposure
  rationale: >-
    Detergent (SDS) exposure impairs the esophageal barrier and induces IL-33
    and eosinophilia in cell-culture and mouse models, but direct human causal
    evidence is lacking. Whether this represents a true initiating exposure in
    patients or an experimentally tractable proxy remains unresolved.
- discussion_id: gap_eoe_eosinophil_symptom_causality
  prompt: >-
    Which eosinophil-dependent versus eosinophil-independent effector mechanisms
    drive dysphagia and fibrostenotic symptoms in EoE?
  kind: KNOWLEDGE_GAP
  status: OPEN
  attaches_to:
  - pathophysiology#Eosinophil Recruitment to Esophagus
  - pathophysiology#Esophageal Fibrosis and Remodeling
  - mechanistic_hypothesis#barrier_antigen_type2_specificity_model
  rationale: >-
    Eosinophil recruitment is a defining histologic and diagnostic axis, but
    eosinophil depletion alone has not consistently translated into symptom
    improvement. The symptom-producing tissue effectors may include epithelial
    remodeling, mast cells, neuromuscular dysfunction, and fibrosis in addition
    to eosinophils.
  evidence:
  - reference: PMID:29372536
    reference_title: "Biological Therapies for Eosinophilic Esophagitis: Where Do We Stand?"
    supports: SUPPORT
    evidence_source: OTHER
    snippet: "Mepolizumab and reslizumab, two anti-IL-5 antibodies, were studied in children and adults with EoE and resulted in reduction of esophageal tissue and blood eosinophils, but no significant reduction in symptoms."
    explanation: Review of biologic therapy trials supports a gap between eosinophil reduction and symptom improvement.
disease_term:
  preferred_term: eosinophilic esophagitis
  term:
    id: MONDO:0005361
    label: eosinophilic esophagitis
references:
- reference: PMID:19596009
  title: Biology and treatment of eosinophilic esophagitis.
  findings: []
- reference: PMID:26857345
  title: Newly developed and validated eosinophilic esophagitis histology scoring system and evidence that it outperforms peak eosinophil count for disease diagnosis and monitoring.
  findings: []
- reference: PMID:29372536
  title: 'Biological Therapies for Eosinophilic Esophagitis: Where Do We Stand?'
  findings: []
- reference: PMID:29980278
  title: Epithelial origin of eosinophilic esophagitis.
  findings: []
- reference: PMID:35899466
  title: Detergent exposure induces epithelial barrier dysfunction and eosinophilic inflammation in the esophagus.
  findings: []
- reference: PMID:40521400
  title: 'Eosinophilic Esophagitis Pathogenesis: All Clear?'
  findings: []
- reference: PMID:30364207
  title: 'Eosinophilic Esophagitis: Review and Update.'
  findings: []
- reference: PMID:36546624
  title: Dupilumab in Adults and Adolescents with Eosinophilic Esophagitis.
  findings: []
📚

References & Deep Research

References

8
PMID:19596009
Biology and treatment of eosinophilic esophagitis.
No top-level findings curated for this source.
PMID:26857345
Newly developed and validated eosinophilic esophagitis histology scoring system and evidence that it outperforms peak eosinophil count for disease diagnosis and monitoring.
No top-level findings curated for this source.
PMID:29372536
Biological Therapies for Eosinophilic Esophagitis: Where Do We Stand?
No top-level findings curated for this source.
PMID:29980278
Epithelial origin of eosinophilic esophagitis.
No top-level findings curated for this source.
PMID:35899466
Detergent exposure induces epithelial barrier dysfunction and eosinophilic inflammation in the esophagus.
No top-level findings curated for this source.
PMID:40521400
Eosinophilic Esophagitis Pathogenesis: All Clear?
No top-level findings curated for this source.
PMID:30364207
Eosinophilic Esophagitis: Review and Update.
No top-level findings curated for this source.
PMID:36546624
Dupilumab in Adults and Adolescents with Eosinophilic Esophagitis.
No top-level findings curated for this source.