From: Microglia dynamics in aging-related neurobehavioral and neuroinflammatory diseases
Type of immune cell | Markers | Promoting factors | Inhibitory factors | Primary function | Condition explored |
---|---|---|---|---|---|
WAM | Apoe, CD63, Clec7a, TMEM119, CX3CR1, P2RY12,Csf1r [195] | CSF1R suppressor [198] | Generates proinflammatory cytokines and display reduced phagocytic activity [196, 199], WAM are precursors to DAM and function in the removal of myelin debris [21, 196] | Aged brain, AD [196] | |
DAM | Lpl, ApoE, TMEM119, P2RY12, CX3CR1, TREM2, CST7, and Axl [200, 201] | Protein accumulation, apoptotic cells, and myelin debris, and needs signaling via type I interferons (IFN-α and IFN-β (IFN-α/β)) and type II interferon (IFN-γ) [200] | TGF-β and NRROS [202] | DAMs reduce the transcriptional signature exclusive to microglia and enhance IFN-feedback genes, lysosomal genes, genes that code lipid-metabolism elements and further exterior receptors and elements related to the damage of synapses and nerve cells [200] | |
LDAM | RAP1B, RAK1, CHBB, TLR2/4, IFN-γ receptor [88] | TREM2-ApoE pathway, phagosome development, innate inflammation [88], generation of nitric oxide and ROS [206] | Triacsin C [88] | LDAMs are deficient in phagocytosis, generate proinflammatory cytokines [88] and synthesize prominent levels of ROS [206] | |
MGnD | Clec7a, Lgals3, Gpnmb, Itgax, app1, Fabp5, Ccl2 [208] | Apoptotic nerve cells, relies on the TREM2-APOE pathway [208] | Relies on the TREM2-APOE signaling [208] | This type of microglia loses sensome actions such as TGFβ signaling[209], MGnD microglia might also be protective and constitute an initial reply to nerve cells damage [210] | Aged brain, neuritic dystrophy, AD, MS, ALS [208] |