(scRNA-Seq), we disclosed that CD83-deficient microglia display an over-activated phenotype. These cells express higher levels of chemokines and create a TNF-α-driven pro-inflammatory milieu, which causes more severe damage in the brain by higher expression of Mmp9. Collectively, we reveal that CD83-deficient microglia are inapt to cope with damage and react with heightened inflammation while showing impaired pro-resolving mechanisms. Our findings provide important insights into the regulation of neuro-inflammatory processes exerted by microglia.
