Collectively, these data identify CD83 as an important regulator of microglial function under neuro-inflammatory conditions. Due to their incapability to properly remove myelin debris, CD83-deficient microglia react with an overshooting production of chemokines, which subsequently attract peripheral immune cells to the inflamed CNS. The interplay with these cells then creates an even more destructive environment, fostering the inflammation and impeding proper resolution of inflammation (Fig. 7). Thus, microglial CD83 expression is not only a marker of cellular activation but an important key regulatory molecule, which keeps neuro-inflammatory processes in check.
