Tbx21, and Il12a) in the spinal cords of CD83ΔMG mice (Fig. 6c–e). Frequencies of IL-17A and GM-CSF producing T cells were unaltered between both groups (Supplementary Fig. 4h). In addition, the distorted ratio of Tregs and Th1 cells was only overt at the site of inflammation (i.e., the CNS) but not in peripheral lymph nodes (Supplementary Fig. 4i). Excessive amounts of IFN-γ are known to impair neuroprotective features of microglia, in part by upregulation of TNF-α production, which interferes with oligodendrogenesis45,46. Thus, we analyzed the expression pattern of Tnf in spinal cords of EAE mice as well as microglia and MDCs sorted from the CNS at the peak of the disease. We disclosed drastically elevated Tnf transcripts in spinal cords of CD83ΔMG mice. Both microglia and MDCs from CD83ΔMG mice expressed significantly higher Tnf levels than cells from control animals (Fig. 6f). TNF-α not only directly affects the oligodendrocyte-dependent remyelination process but also promotes the destruction of the blood-brain-barrier by 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
