From:  Cellular state transitions in neuroimmune disorders

 Therapeutic strategies targeting cellular state transitions in neurological disease.

Therapeutic strategyMolecular targetTarget cell populationMechanism of actionDisease context
Complement pathway inhibitionComplement proteins C1q, C3Microglia, synapse-associated immune signaling pathwaysReduces complement-mediated synaptic pruning and inflammatory activationAlzheimer’s disease, multiple sclerosis [241, 242]
Immune checkpoint modulationPD-1/PD-L1 signaling axisT lymphocytes, microgliaModulates immune activation and inflammatory signaling by regulating immune checkpoint pathwaysStroke, neuroinflammatory disorders [243, 244]
Triggering receptor expressed on myeloid cells 2 (TREM2) modulationTREM2MicrogliaEnhances microglial metabolic activity, phagocytosis, and responses to neurodegenerative pathologyAlzheimer’s disease and related neurodegenerative diseases [245, 246]
Colony-stimulating factor 1 receptor (CSF1R) inhibitionCSF1RMicrogliaAlters microglial survival and proliferation, thereby modulating microglial population dynamics and inflammatory responsesNeurodegenerative disease models, neuroinflammation [247, 248]
Cytokine pathway inhibitionIL-6, TNF, interferon signaling pathwaysMicroglia, astrocytes, immune cellsReduces inflammatory signaling and downstream neuroimmune activationStroke, neuroinflammatory disorders [249, 250]