inducing the expression of matrix metalloproteinase 9 (MMP9), for instance in astrocytes47. Thus, we assessed the spinal cords of EAE mice for the expression of Mmp9 and detected significantly elevated transcript levels in CD83ΔMG mice, demonstrating that CD83-deletion in microglia leads to more severe disruptive processes in the inflamed CNS (Fig. 6g). Other pro-inflammatory transcripts like Il6 and Il23a were not differently expressed in the spinal cord between both groups (Supplementary Fig. 4j), proving that the elevated expression of TNF-α and MMP9 is not a result of generally augmented inflammation in the CD83ΔMG CNS.
