Above, we have reported that CD83-deficient microglia acquire a highly activated phenotype during EAE and produce chemotactic signals to attract monocytic cells, which ultimately differentiate into APCs. Importantly, the chemokines Ccl4 and Ccl5, which recruit pathogenic T cells44, were not only significantly elevated in microglia from CD83ΔMG mice but also in sorted MDCs (Supplementary Fig. 4g). Monocyte-derived APCs are the key cells that interact with encephalitogenic T cells and drive neuroinflammation11, and thus, we next investigated the T cell subsets infiltrating the CNS of EAE animals. Flow cytometric analyses revealed that the percentage of CD25+/FoxP3+ CD4+ T cells (i.e., regulatory T cells) was significantly diminished in the CNS of CD83ΔMG mice (Fig. 6a, b). By contrast, the CNS of these animals contained more IFN-γ producing CD4+ T cells, which correlated with strikingly increased expression levels of Th1-related transcripts (i.e., Ifng, 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
