Fig. 5
Removal of IFNAR1 in APPSWE/PS1ΔE9 mice shifts the microglial phenotype to an anti-inflammatory state. a Q-PCR of cortical tissue isolated from 9 month old wildtype, IFNAR1−/−, APPSWE/PS1ΔE9 and APPSWE/PS1ΔE9 x IFNAR1−/− littermate controls analyzing iNOS, CD11b, CD32 and CD33 pro-inflammatory glial marker expression levels. b Q-PCR of cortical tissue isolated from 9 month old wildtype, IFNAR1−/−, APPSWE/PS1ΔE9 and APPSWE/PS1ΔE9 x IFNAR1−/− littermate controls analyzing TGFβ, YM1, ARG1, CD206, CCL22 and TREM2 anti-inflammatory glial marker expression levels. c Immunoblot of Tris–HCl soluble cortical protein lysates isolated from 9 month old wildtype, IFNAR1−/−, APPSWE/PS1ΔE9 and APPSWE/PS1ΔE9 x IFNAR1−/− mice using anti-SOCS-3. Comparative summaries of d Pro-inflammatory and e anti-inflammatory glial marker expression in APPSWE/PS1ΔE9 and APPSWE/PS1ΔE9 x IFNAR1−/− mice are displayed. For Q-PCR, all samples were normalized back to the Ct value of the housekeeping gene GAPDH (ΔCt). The mRNA of the variant genotype groups were then expressed relative to their gene-specific wildtype littermate controls. For western blotting, immunodetection of β-actin was used to ascertain loading quantities. Data are displayed as mean alone or as box plots described in the statistical analysis section in Materials and Methods (n = 9 per genotype; •represents outlier value; *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001). See Additional file 2: Table S1 for further analysis