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Chunk #18 — Results — Deletion of CD83 in microglia exacerbates autoimmune neuroinflammation

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Microglial expression of CD83 governs cellular activation and restrains neuroinflammation in experimental autoimmune encephalomyelitis.
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and composition of immune cells (CD45+). Microglia from CD83wtCre EAE mice had significantly higher CD83 surface levels than those derived from CD83ΔMG mice (Supplementary Fig. 4a), thus confirming the KO efficiency. We also verified the KO-specificity in sorted microglia on mRNA level and proved that the KO does not affect infiltrating, peripheral MDCs at the peak of disease (Supplementary Fig. 4b). When assessing the cellular composition of the CNS, we observed a striking infiltration of immune cells of the myeloid lineage (CD45high/CD11b+) in CD83ΔMG mice, which were further stratified into infiltrating neutrophil granulocytes (Ly6G+/Ly6Clow), monocytes (Ly6G/Ly6Chigh), and monocyte-derived cells (MDCs, Ly6G-/Ly6Clow) (Fig. 3f). While the frequency of microglial cells (CD45low/CD11b+) was significantly diminished in CD83ΔMG mice, the percentage of monocytes and MDCs increased (Fig. 3g). Most of the MDCs expressed high levels of MHC-II and CD11c and were therefore termed monocyte-derived DCs (moDCs), whose proportion among all immune cells was also significantly elevated in CD83ΔMG mice compared with controls (Fig. 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