cytokine
IL-13
Type 2 tissue remodeling cytokine for mucus, barrier repair, fibrosis drift, and airway reactivity
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.
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.
Chronicity
Memory, priming, fibrosis, exhaustion, remodeling, or other time-dependent drift.
Cascade viewer
Source → signal → tissue behavior
Sources
Signal
IL-13
Targets and effects
Graph neighborhood
Direct relationships
Arrow shows upstream source toward receiving target.
Mucus, airway reactivity, and tissue remodeling
Context link: no causal arrow.
Tissue remodeling arm of type 2 inflammation
Arrow shows upstream source toward receiving target.
TH2 IL-13 drives mucus and tissue remodeling
Arrow shows upstream source toward receiving target.
ILC2 programs can produce IL-13 during alarmin-rich allergic and repair states
Cytokine ecology
Signal Role
IL-13 acts on epithelial and stromal compartments to drive mucus, smooth muscle reactivity, collagen programs, and type 2 remodeling.
Pathway
Source Cells
Target Cells
Inflammatory Role
Amplifies allergic tissue remodeling, mucus, airway hyperreactivity, and fibrotic repair tone.
Regulatory Role
Supports helminth expulsion and wound repair when self-limited.