cell
Microglia
CNS-resident macrophage lineage controlling synapses, injury response, sickness signaling, and neuroinflammation
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
Graph neighborhood
Direct relationships
Primary CNS-resident immune cell
Network behavior
Systems Overview
Microglia maintain neural tissue, prune synapses, sense infection or injury, and adopt states that range from homeostatic surveillance to inflammatory, repair, or degenerative programs.
Lineage
Origin
Yolk-sac-derived macrophage lineage seeded into the CNS during development
Transcription factors: PU.1, IRF8, SALL1, MEF2C
Lifecycle Visualizer
embryonic
Developmental seeding
CNS niche occupation
lifelong
Homeostatic surveillance
Process motility and synapse monitoring
hours-days
Activated transition
Debris and cytokine response
weeks-years
Primed state
Lowered threshold in aging or chronic inflammation
Activation and Suppression
Surface and Secreted Signals
Metabolic State
Programs
Acute: Rapid sensing of ATP, debris, and cytokines shifts motility and inflammatory output.
Chronic: Persistent debris, aging, and systemic inflammation can create primed or disease-associated states.
Tissue Roles
CNS: Synaptic pruning, debris clearance, immune surveillance, repair, and neuroinflammatory amplification.
gut: Indirectly shaped by microbial metabolites and vagal/systemic inflammatory signals.
vasculature: Interacts with barrier cells and perivascular macrophage compartments.
Disease Associations
Clinical Pearls
- Microglial activation is a state spectrum, not a single on/off switch.
- Peripheral inflammation can be felt centrally through cytokines, barrier signaling, and neural afferents.
- Sleep is a major neuroimmune regulator because clearance and inflammatory thresholds change over time.