Fig. 5

The Sensome is downregulated in human microglia from glioblastoma patients. a Analysis of published bulk RNAseq data from CD11B^pos microglia harvested from postmortem human brains (control) or glioblastoma patients identifies differences based on sample group as well as heterogeneity between glioblastoma derived cells. b Glioblastoma microglia showed significantly reduced levels in 32% of genes versus 12% upregulation, indicating reduced overall capability of sensing of tumor cells and tumor-derived danger signals in human glioblastoma microglia. Further analysis of published human glioblastoma single-cell microglia data identified similar results. c Expression levels of TMEM119, P2RY12, GPR34, OLFML3, SCL2A5, SALL1, and ADORA3 for microglia and CRIP1, S100A8, S100A9, ANXA1, and CD14 for macrophages were used to identify individual microglia and macrophages cells isolated at either the core or periphery of the glioblastoma mass. d At a single-cell level, 15% of genes are significantly upregulated (genes in red), and 48% of the human sensome genes are significantly downregulated (genes in blue) when comparing microglia at the core to microglia in the periphery of the glioblastoma mass again indicating reduced capability of sensing of tumor cells and tumor-derived danger signals in human glioblastoma microglia. e Schematic illustration showing the anti-tumor ability of microglia after EV uptake by simultaneous reduction of the sensing capacity and host defense as well as an increased homeostatic function. This pathway is ultimately required for glioblastoma growth. Asterisk (*) indicates significant (multiple testing adjusted p value < 0.05) differential expression. Error bar represents the SEM, bar represents the mean, and dots display individual measurements (a, b: control n = 5, glioblastoma n = 8, C, D microglia core n = 365, microglia periphery n = 574)