Figure 4.

Analysis of the influence of disease and IFNAR1 on microglial activation and inflammatory, phagocytic and lysosomal gene products. Top panel; distribution of microglia is shown in the hippocampi of normal brain homogenate (NBH) and ME7 animals (18 weeks postinoculation) on IFNAR1‐deficient and wild‐type backgrounds, and insets illustrate the activated morphology visible in ME7 animals of both genotypes (scale bar 200 μm). Thereafter, quantitative PCR was used to assess the expression, in NBH and ME7 mice, in wild‐type and IFNAR1 deficient genotypes, of transcripts for multiple neuroinflammation‐associated mediators (a) Il1b, (b) Tnf, (c) Tgfb1, (d) Il10, (e) inducible nitric oxide synthase; Nos2, (f) Arg1, (g) triggering receptor expressed on myeloid cells 2; Trem2, (h) macrosialin; Cd68, complement pathway components: (i) C1qa, (j) C3, (k) Itgam (cd11b), (l) Msr1 (scavenger receptor A2), NADPH oxidase subunits (m) Cybb (gp91phox), (n) Cyba (p22phox) and lysosomal cathepsins (o) Ctss (Cathepsin S), (p) Ctsd (Cathepsin D). All data are plotted as mean ± SEM with n = 4 (NBH in WT or IFNAR1^−/−) and n = 5 (ME7 in WT or IFNAR1^−/−) and analyzed by two‐way anova with disease and strain as between subjects factors. Significant differences are denoted *p < 0.05, **p < 0.01, and ***p < 0.001 by Bonferroni post hoc analysis