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. 2017 Sep 28;8:717. doi: 10.1038/s41467-017-00769-0

Fig. 2.

Fig. 2

Microglia of adult mice express an ageing-like phenotype following chronic exposure to IFN-β. a Schematic presentation of the experimental design for testing the effect of IFN-I overexpression on microglia. b Representative image of the choroid plexus in the lateral ventricle (LV; contralateral to the intracerebroventricular administration site), expressing GFP following AAV-mediated infection (GFP in green, Claudin-1 marking epithelial tight junctions in red, nuclear Hoechst staining in blue). c Volcano plot showing the fold change and significance of gene expression values between microglia from IFN-I-overexpressing (AAV-IFNβ) and control (AAV-CTRL) adult mice (P < 0.05; unpaired t-test, n = 2–3 per group). d Fraction of differentially expressed genes from the microglia of IFN-I-overexpressing mice that were increased (left) or decreased (right) in aged mice (relative to young). Dashed line indicates the expected distribution of genes. Significance of enrichment or depletion *P = 0.0008, # P = 0.0011; hypergeometric test. e Representative micrographs of Iba-1 staining in microglia in the hippocampus of mice infected with AAV-IFNβ or AAV-CTRL. f Quantification of Iba-1 staining intensity and analysis of microglial morphology reveals IFN-I-induced microgliosis in the hippocampus. **P < 0.01, *P < 0.05; unpaired t-test, n = 5 per group, the results are representative of two independent experiments