Fig. 4: Exacerbated immune responses after EAE induction in NR3C1 cKO mice.
From: NR3C1-mediated epigenetic regulation suppresses astrocytic immune responses in mice
a Schematics of experiments for the generation of NR3C1 cKO mice and autoimmune challenges. b The number of NR3C1+ astrocytes in Cre− control and NR3C1 cKO mice at P17. Mice were used with n = 3 for Cre− control, n = 5 for NR3C1 cKO. Data are shown as mean ± standard error of the mean (SEM) and are analyzed by one-sided unpaired t test (P < 0.0001). c Heatmap representing DEGs of NR3C1 cKO astrocytes at P17 under naive conditions. d Bar graphs showing the overlapping ratio between DEGs of NR3C1 cKO astrocytes and astrocyte developmental stage-specific DEGs. Hypergeometric p value are shown together (Up-P7, P = 1.64 × 10−5; Up-P17, P = 0.010; Down-P17, P = 2.72 × 10−13; Down-P30, P = 1.31 × 10−7). e Top 5 enriched MSigDB Hallmark pathways of DEGs in NR3C1 cKO astrocytes. f GFAP expression in the corpus callosum. Bar graphs showing the area of GFAP expression compared between Cre− control and NR3C1 cKO mice under naive conditions (P = 0.749) and at the peak of EAE (P = 4.65 × 10−2). Mice were used with n = 3 or n = 7 for Cre− control and n = 4 or n = 7 for NR3C1 cKO at naive or EAE peak stage, respectively. Data are shown as mean ± SEM and were analyzed by a two-sided unpaired t test. g EAE clinical score in Cre− control mice (n = 12) and NR3C1 cKO mice (n = 10). Two-way ANOVA, P < 0.0001. Data are shown as mean ± SEM. Scale bars, 20 μm. h IBA1 expression in corpus callosum at the EAE peak (P = 0.056). Mice were used with n = 7 for Cre− control and 7 for NR3C1 cKO. Data are shown as mean ± SEM and were analyzed by two-sided unpaired t test. i The number of CD4+ T cells in corpus callosum at the EAE peak (P = 1.6 × 10−3). Mice were used with n = 7 for Cre− control and 7 for NR3C1 cKO. Data are shown as mean ± SEM and were analyzed by two-sided unpaired t test. Scale bars, 40 μm. j, k GFAP expression (j P = 2.09 × 10−2) and the number of CD45+ cells (k P = 6.50 × 10−3) in the spinal cord at the peak of EAE. Mice were used with n = 3 for Cre− control and n = 4 for NR3C1 cKO. Data are shown as mean ± SEM and were analyzed by two-sided unpaired t test. Scale bars, 100 μm (j) and 50 μm (k). Source data are provided as a Source Data file.
