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. 2017 Jun 23;9:207. doi: 10.3389/fnagi.2017.00207

Figure 1.

Figure 1

Microglia in the prion-diseased brain. In the healthy brain, microglia constantly surveil their microenvironment for any disturbance of brain homeostasis and are kept in this surveiling state by signals mainly originating from healthy neurons. The microglial population is maintained by local self-renewal mediated via CSF1R and its ligands CSF1 and IL-34. In the context of neurodegeneration and protein accumulation present in the prion-diseased brain, the microglial response is characterized by functional changes involving increased proliferation, an inflammatory activation and the removal of apoptotic neurons. CX3CL1, C-X3-C motif chemokine ligand 1; CX3CR1, C-X3-C motif chemokine receptor 1; CD200, Cluster of differentiation 200; CD47, Cluster of differentiation 47; SIRPα, Signal regulatory protein α; CSF1R, Colony stimulating factor 1 receptor; CSF1, Colony stimulating factor; IL-34, Interleukin 34; MFGE8, Milk fat globule-EGF factor 8 protein; ROS, Reactive oxygen species; NOX2, Nicotinamide adenine dinucleotide phosphate-oxidase (NADPH) oxidase 2; NFκB, Nuclear factor kappa-light-chain-enhancer of activated B cells; STAT1/3, Signal transducer and activator of transcription 1/3; TNFα, Tumor nerosis factor α; IL-1β, Interleukin 1β; CCL2, C-C motif chemokine ligand 2; TGFβ, Transforming growth factor β; PrPSc misfolded prion protein (scrapie).