cell
Basophil
Circulating type 2 granulocyte linking IgE, IL-4, parasites, allergy, and early TH2 amplification
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.
Local map
Relationship field
Arrows point from the upstream source toward the receiving target. Restraint edges use a bar; association edges stay dashed because they are not causal arrows.
Basophils can provide early IL-4 in IgE, helminth, and type 2 barrier contexts
Read as source produces or releases the target signal.
What this relationship means
Read this as output: Basophil can release IL-4, which then carries the next part of the signal.
Effect of source
Basophil is the producing cell or node.
Effect on target
IL-4 is the released mediator to follow downstream.
Use with caution
Release edges show possible biology, not measured patient levels.
System effect
Basophil releases IL-4; the mapped axes are inherited mainly from the released signal.
Inflammation
Inflammatory alarm, recruitment, mediator release, or tissue-damaging amplification.
Tissue
Organ, barrier, stromal, vascular, or local niche behavior.
Metabolism
Energy allocation, glycolysis, mitochondrial strain, lipid signaling, or nutrient-sensitive behavior.
Axes are mapped cues from Atlas data, not clinical predictions.
Evidence context
Curated edge, reviewed endpoints, and mapped external anchors.
Interleukin-4 and Interleukin-13 signaling
R-HSA-6785807 - checked 2026-06-28
Graph neighborhood
Direct relationships
Arrow shows upstream source toward receiving target.
Basophils can provide early IL-4 in IgE, helminth, and type 2 barrier contexts
Context link: no causal arrow.
Basophils are part of the IgE/type 2 allergic amplification circuit
Network behavior
Systems Overview
Basophils are rare blood granulocytes that carry FcεRI, release histamine and IL-4/IL-13, and can amplify type 2 immunity at the boundary between allergy, helminth defense, and barrier alarm.
Lineage
Origin
HSC -> granulocyte-monocyte progenitor -> basophil progenitor -> mature circulating basophil
Transcription factors: GATA2, C/EBPα, MITF-associated programs, STAT5
Lifecycle Visualizer
days
Basophilopoiesis
IL-3-sensitive granulocyte development
days
Circulation
Blood sentinel with FcεRI
minutes-hours
Activation
Degranulation and cytokine release
hours-days
Resolution
Short-lived effector contraction
Activation and Suppression
Surface and Secreted Signals
Metabolic State
Programs
Acute: IgE or cytokine stimulation triggers degranulation, histamine release, and early IL-4 output.
Chronic: Repeated type 2 cytokine and antigen exposure can sustain basophil activation markers and allergic amplification.
Tissue Roles
blood: Rare circulating granulocyte that can indicate type 2 activation context.
lung: Can amplify allergic airway responses through IL-4/IL-13 and histamine biology.
skin: Participates in wheal, itch, and late-phase allergic inflammation.
gut: Contributes to helminth and food-allergy type 2 ecology.
lymphoid: Can support early TH2 polarization through IL-4-rich instruction.
Disease Associations
Clinical Pearls
- Basophils are easy to miss because they are rare, but they are central to IgE/type 2 amplification.
- CD63 and CD203c are activation markers used in basophil activation concepts.
- Basophils can help explain early IL-4 tone before a full TH2 tissue program is established.