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Chunk #21 — 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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Projection (UMAP) to visualize clustering (Fig. 4b). We obtained six clusters, two of which were associated with cells from healthy animals (Gpr34+ and Ccl4+) while the other four cluster largely contained cells from EAE animals (Fig. 4c). Cells in the Gpr34+ subset expressed high levels of Tmem119, P2ry12, Siglech, and Sall1, thus representing mainly homeostatic microglia. We also identified two EAE-specific clusters rich in MHC-II related transcripts (H2-Aa, H2-Ab1, CD74), which could be distinguished by high expression of Apoe (Fig. 4d). Other clusters that were exclusively present in EAE-derived cells contained genes associated with proliferation (Mki67, Top2a) or chromatin-assembly (Hmgb2, H2afz, Stmn1). When assessing the distribution of Cd83 expression, we noticed that while being homogenously present in most identified clusters, Cd83 was particularly expressed in cells of the Ccl4+ and MHC-II/Apoe+ cluster (Fig. 4e, Supplementary Fig. 5c). Additionally, we confirmed that Cd83 expression was absent in isolated cells from CD83ΔMG (Supplementary Fig. 5c).