Fig. 3

STRING network analysis of the top 57 genes predominantly expressed by microglia that are significantly increased at ≥3.0-fold in the brain during prion disease (a). Markov clustering indicated 4 groups of interacting protein networks. The largest group indicated by red nodes (red oval) centers around the hetero-dimeric integrin receptor CD11c/18, which is encoded by Itgax and Itgb2 (black dotted oval). Experimentally determined interactions are indicated by pink lines, interactions that are curated in databases (Reactome, KEGG, etc.) are indicated by blue lines, and proteins that are homologues are indicated by purple lines. Solid lines indicate interactions within clusters, and dotted lines indicate interactions between clusters. Only connected nodes are shown, with disconnected nodes comprising 27 genes removed from view. The upregulated genes used for this analysis are found in Table 2 and Additional File, Supplementary Dataset 2. Venn diagrams comparing significantly altered genes at different times (80, 100, and ~ 157 days) post-prion infection to the gene expression pattern of microglia associated with neurodegeneration (MGnD) (b and c). The MGnD phenotype is characterized by changes in 96 transcripts. Twenty-eight inflammatory genes are increased in the MGnD phenotype (b), but only 13 of these inflammatory genes are significantly increased with time during prion infection. Sixty-eight homeostatic microglial genes are decreased in the MGnD phenotype (c), but only one of these homeostatic microglial genes is significantly decreased during prion disease. The genes altered at 80, 100, and ~ 157 dpi achieved our criteria for significance (either ≥2-fold or ≤ − 2-fold, with a p value ≤0.05). The details of expression changes in the 96 MGnD microglia-associated transcripts during prion infection can be found in Additional File, Tables S2 and S3