cell
Innate Lymphoid Cell
Tissue-resident innate lymphocyte family that mirrors helper T-cell programs without antigen-specific receptors
Review layer
Last reviewed 2026-05-17
Systems teaching draft. Content is structured for education and graph expansion, with formal source tagging ready for the next review pass.
State signature
Systems profile
System effects
Primary mapped axes from existing Atlas data.
Tissue
Organ, barrier, stromal, vascular, or local niche behavior.
Metabolism
Energy allocation, glycolysis, mitochondrial strain, lipid signaling, or nutrient-sensitive behavior.
Inflammation
Inflammatory alarm, recruitment, mediator release, or tissue-damaging amplification.
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.
Selected relationship
IL-33 activates ILC2-type barrier responses with IL-5, IL-13, and amphiregulin output
Read as source increases target activity, recruitment, or threshold crossing.
What this relationship means
Read this as IL-33 influencing Innate Lymphoid Cell; the arrow names the direction, while the details explain the likely system domain.
Effect of source
IL-33 is the upstream signal or context.
Effect on target
Innate Lymphoid Cell is the receiving node whose behavior may shift.
Use with caution
Use this as a map-reading aid, not as diagnosis, triage, treatment guidance, or a risk score.
System effect
IL-33 influences Innate Lymphoid Cell; the axes below show which mapped systems carry that relationship.
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-33
O95760 - checked 2026-06-28
Graph neighborhood
Direct relationships
Arrow shows upstream source toward receiving target.
IL-33 activates ILC2-type barrier responses with IL-5, IL-13, and amphiregulin output
Arrow shows upstream source toward receiving target.
ILC2 programs can produce IL-13 during alarmin-rich allergic and repair states
Network behavior
Systems Overview
Innate lymphoid cells sense epithelial and cytokine cues and rapidly produce type 1, type 2, or type 3 cytokines, shaping barrier defense, allergy, repair, and mucosal ecology.
Lineage
Origin
HSC -> common lymphoid progenitor -> innate lymphoid progenitor -> ILC1, ILC2, ILC3, or NK-like states
Transcription factors: ID2, T-bet, GATA3, RORγt, PLZF
Lifecycle Visualizer
weeks
ILC commitment
Innate lymphoid fate
developmental-weeks
Tissue seeding
Barrier-resident niche
hours
Rapid activation
Cytokine release
days-weeks
Plasticity or resolution
Context-dependent ILC state shift
Activation and Suppression
Surface and Secreted Signals
Metabolic State
Programs
Acute: Barrier cytokines rapidly trigger cytokine release without antigen-specific priming.
Chronic: Persistent alarmins or dysbiosis can keep ILC programs active and remodel tissue.
Tissue Roles
gut: ILC3 IL-22 supports barrier integrity; dysregulation can amplify inflammation.
lung: ILC2 produces IL-5/IL-13 during alarmin-rich allergy or repair responses.
skin: Supports barrier defense, itch/type 2 loops, and repair.
adipose: ILC2-like programs can support type 2 metabolic homeostasis.
lymphoid: Participates in tissue organization and barrier immune tone.
Disease Associations
Clinical Pearls
- ILCs are the fast tissue version of helper logic: TH1-like, TH2-like, or TH17-like without TCR specificity.
- ILC2s help explain allergy and repair before adaptive memory fully enters the loop.
- ILC3s link microbiome and epithelial IL-22 biology to barrier resilience.