cytokine
IL-4
TH2 polarization signal for IgE class switching, alternatively activated macrophages, and barrier allergy
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.
Neuroimmune
Nerve, neuropeptide, autonomic, microglial, pain, itch, fatigue, or sickness-behavior coupling.
Metabolism
Energy allocation, glycolysis, mitochondrial strain, lipid signaling, or nutrient-sensitive behavior.
Cascade viewer
Source → signal → tissue behavior
Sources
Signal
IL-4
Targets and effects
Graph neighborhood
Direct relationships
Arrow shows upstream source toward receiving target.
Type 2 barrier amplification
Arrow shows upstream source toward receiving target.
TH2 polarization through STAT6 and GATA3
Arrow shows upstream source toward receiving target.
Allergic airway type 2 loops
Arrow shows upstream source toward receiving target.
Type 2 tissue amplification
Arrow shows upstream source toward receiving target.
IL-4 promotes IgE class switching and type 2 antibody context
Arrow shows upstream source toward receiving target.
IL-4 drives STAT6/GATA3 type 2 helper differentiation
Cytokine ecology
Signal Role
IL-4 is a type 2 cytokine that pushes B cells toward IgE and T cells toward TH2 identity while shaping repair-biased macrophage programs.
Pathway
Source Cells
Target Cells
Inflammatory Role
Amplifies allergic sensitization and type 2 barrier inflammation.
Regulatory Role
Can redirect macrophages toward repair and helminth containment rather than cytotoxic inflammation.