only a significant increase in eGFP-reporter activity but also elevated CD83 surface levels in microglia from inflamed CNS (Fig. 2b, c). It has been reported that activated microglia adopt a CD11c+/MHC-II+ phenotype during neuroinflammation28, and when we examined the phenotype of microglia during neuroinflammation in further detail, we observed that CD83 expression was highest in such activated cells of the spinal cord and the brainstem region, followed by microglia of the cerebellum (Fig. 2d). Additionally, expression of CD83 also increases in activated cortical microglia albeit to a lesser extent than in cells from caudal brain regions (Fig. 2e). These flow cytometry data were further corroborated with two-photon microscopy showing co-localization of eGFP and the microglial marker P2RY12, especially in cells of caudal brain regions (Supplementary Fig. 1c, d). Interestingly, monocytes, which do not express CD83 under homeostatic conditions, acquired eGFP signal, whereas granulocytes, although massively infiltrating the inflamed brain, do not express elevated levels of CD83 during disease (Supplementary Fig. 1e, f). Cd83-promoter activity was exceptionally high in monocytes upon transition to an APC-phenotype (CD11c+/MHC-II+), which implies that CD83 expression is not exclusively induced in activated microglia during neuroinflammation. However, the eGFP signal in microglia further increases during the recovery
