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. Author manuscript; available in PMC: 2019 Oct 1.
Published in final edited form as: Brain Behav Immun. 2018 Jul 17;73:133–148. doi: 10.1016/j.bbi.2018.07.012

Figure 3. Microglial phenotype is regulated by other cells in the CNS.

Figure 3.

In healthy CNS, steady-state microglial quiescence is maintained by signaling with neurons (neuron CD200L to microglia CD200R; neuron CX3CL1 to microglia CX3CR1) and astrocytes (e.g., TGF-β signaling limits microglial activation). Dysregulation of these cell-cell interactions can contribute to microglial priming. In addition, hematogenous immune cells - which typically have no/very limited access to the CNS - can invade CNS tissue in stress and aging. Pro-inflammatory subtypes of infiltrating cells, such as macrophages, can signal to microglia to elicit priming and/or activation. Anti = anti-inflammatory actions; Pro = pro-inflammatory actions.