3h). While there was also a significantly increased proportion of cells of the lymphoid lineage (CD45high/CD11b−), we observed no differences in the frequency of neutrophil granulocytes (Supplementary Fig. 4c). Since the aggravated EAE phenotype in CD83ΔMG mice was accompanied by a heightened influx of monocytic cells, we next investigated the production of Ccl2, which is a prerequisite for a regular development of EAE symptoms34. Compared to control cells, the expression of Ccl2 was most strikingly elevated in CD83ΔMG mice (Fig. 3i). We also investigated other chemokines, which are important for EAE development35, and found that CD83cKO microglia expressed significantly higher levels of Ccl4 and Ccl5 at the peak of disease (Fig. 3i). Interestingly, analysis of Ccl3 expression showed no difference between CD83ΔMG and controls, demonstrating that chemokine production was not generally elevated due to microglial over-activation (Supplementary Fig. 4d).
