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Chunk #26 — Results — Microglial CD83-deficiency causes an over-activated phenotype supportive of pro-inflammatory pathways

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Microglial expression of CD83 governs cellular activation and restrains neuroinflammation in experimental autoimmune encephalomyelitis.
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Ctsb, which are associated with the highly activated phenotype (Fig. 5f), whereas control cells rather expressed genes implicated in early inflammatory activation (Adamts1, Btg1, Egr1, Large1)40,41. When evaluating the Gene Ontology Biological Process terms, we discovered that gene expression pattern in CD83cKO microglia strongly correlates with pathways associated with APC activation and leukocyte-mediated immunity (Fig. 5g). Contrarily, WT cells showed a strong association with pathways involved in cell division. By conducting enrichment analysis of genes whose expression highly correlates with Cd83 in microglia during EAE, we detected a significant enrichment of processes that are involved in the negative regulation of the immune system and the response to external stimuli (Supplementary Fig. 5f).