in microglia isolated from CD83ΔMG mice compared to controls (Fig. 5b). Microglia typically lose expression of signature genes such as Tmem119 during the transition from homeostatic to disease-associated phenotypes11,37. Interestingly, CD83-deficient microglia, despite being more activated, exhibited reduced surface levels of CD86 and MHC-II, which is in line with the anticipated role of CD83 in inhibiting MARCH-1-dependent degradation of both molecules (Supplementary Fig. 4e)15.
