clinical pattern
TH2 / Allergic Pattern
IgE, mast cells, eosinophils, epithelial alarmins, and type 2 repair biology
Review layer
Last reviewed 2026-05-17
Use as a systems teaching model for type 2/allergic inflammation. Clinical interpretation depends on phenotype, tissue context, exposure history, and biomarkers.
Provenance layer
External context
Curated external IDs add pathway and protein context around Atlas content. They do not update the graph automatically and they are not patient-specific interpretation.
Appears in response traces
State signature
Systems profile
System effects
Primary mapped axes from existing Atlas data.
Tissue
Organ, barrier, stromal, vascular, or local niche behavior.
Inflammation
Inflammatory alarm, recruitment, mediator release, or tissue-damaging amplification.
Metabolism
Energy allocation, glycolysis, mitochondrial strain, lipid signaling, or nutrient-sensitive behavior.
No direct axis cue is mapped for this node yet.
Pattern signature
Recognizable immune constellation
Signals
01IL-4
IL-5
IL-13
TSLP
IL-33
IgE
Cells
02mast cells
eosinophils
basophils
T cell subsets
ILC2
Tissues
03lung
skin
gut
Restraint
04IL-10
Tregs
SCFAs
vagal tone
barrier restoration
Graph neighborhood
Direct relationships
Context link: no causal arrow.
Effector and amplifier cell
Context link: no causal arrow.
Eosinophil arm of type 2 inflammation
Context link: no causal arrow.
Tissue remodeling arm of type 2 inflammation
Context link: no causal arrow.
TH2 cells are the adaptive helper engine of type 2 allergic ecology
Context link: no causal arrow.
Basophils are part of the IgE/type 2 allergic amplification circuit
Pattern logic
Interpretation
Look for barrier disruption, epithelial alarmins, IgE sensitization, neurogenic amplification, and repair/fibrosis drift.