From:  Cellular state transitions in neuroimmune disorders

 Triggers of cellular state transitions in the central nervous system.

Trigger categoryExample molecules/signalsSourceCellular targetsFunctional consequence
Damage-associated molecular patterns (DAMPs)HMGB1, extracellular ATP, extracellular DNA fragments, heat-shock proteinsInjured neurons, damaged glial cells, mitochondrial damage, extracellular matrix breakdownMicroglia, astrocytes, endothelial cellsActivation of pattern-recognition receptors, induction of inflammatory signaling, initiation of neuroimmune responses [77, 78]
Pro-inflammatory cytokinesIL-1β, TNF, IL-6, IFN-γMicroglia, astrocytes, endothelial cells, infiltrating immune cellsMicroglia, astrocytes, neurons, immune cellsActivation of inflammatory signaling pathways, modulation of gene-expression programs, promotion of cellular activation states [79, 80]
ChemokinesCCL2, CXCL10, CX3CL1 and related chemokinesActivated glial cells, endothelial cells, infiltrating immune cellsMicroglia, monocytes/macrophages, T cellsRegulation of immune-cell recruitment, migration, and positioning within neural tissue [81]
Metabolic stress signalsAltered glucose metabolism, mitochondrial dysfunction, lipid metabolism shiftsNeurons, glial cells experiencing metabolic imbalanceMicroglia, astrocytes, neural stem cellsActivation of immunometabolic pathways and modulation of inflammatory signaling [82, 83]
Oxidative stressReactive oxygen species, mitochondrial oxidative productsMitochondrial dysfunction, inflammatory signaling, cellular injuryNeurons, microglia, astrocytesModification of signaling proteins, activation of inflammatory transcriptional pathways, amplification of immune responses [84, 85]
HypoxiaReduced oxygen availability, hypoxia-inducible signaling pathwaysIschemia, vascular dysfunction, tissue injuryMicroglia, astrocytes, endothelial cellsActivation of hypoxia-responsive transcription programs and metabolic adaptation pathways [86, 87]