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Fig. 3 | Journal of Neuroinflammation

Fig. 3

From: SLAMF7 modulates B cells and adaptive immunity to regulate susceptibility to CNS autoimmunity

Fig. 3

SLAMF7 restrains CNS myeloid cell activation, regulates adaptive immune responses, and controls CNS B cell activation. A Top, UMAP of all CNS microglia in WT mice during EAE with FlowSOM-defined clusters differentially colored. Bottom, histograms of activation marker expression on microglia subsets from above. Notably, activated microglia have very high protein-level expression of SLAMF9. B–D Expression of CD80 on microglia (B), DCs (C), and BAMs (D) in the CNS in WT and SLAMF7−/− mice at steady state and during EAE. E, F Memory T cell ELISpot assay for IFNγ (E) and IL-17 (F) production from rhMOG35–55 peptide-stimulated splenocytes derived from naïve and rhMOG35–55-treated WT and SLAMF7−/− mice. Cells were cultured without stimulation or in the presence of the rhMOG35–55 peptide for 24 h. Shown below each bar graph are wells containing splenocytes from EAE mice stimulated with MOG peptide. G ELISA of MOG35–55-specific total IgG using plasma derived from WT (n = 8) and SLAMF7−/− (n = 7) mice subjected to EAE with rhMOG35–55. H Heatmap of differential marker expression on all CNS immune cell subsets from WT and SLAMF7−/− mice during EAE (rmMOG1–125) with an FDR < 0.05. Adjusted p-values displayed on the right of each row. I Temporal expression of various plasma cytokines/chemokines in WT (n = 6) and SLAMF7−/− mice (n = 8) during EAE induced with rmMOG1–125. Groups in B–D compared using a one-way ANOVA with Tukey’s multiple comparison test. Groups in E, F compared with a two-way ANOVA with FDR correction for multiple comparisons via Benjamini and Hochberg method. Groups in H compared with a GLMM. Groups in I compared using a mixed-effects model with Sidak’s post hoc test implemented through GraphPad Prism and representative of a single experiment. *p < 0.05, **p < 0.01, ****p < 0.0001. BAMS, border-associated macrophages; MdCs, myeloid-derived cells

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