Fig. 2

Patient-derived iMGs carrying GRN variants represent an activated inflammation state and defective phagocytosis. A Fluorescence images of CD68 (green, reactive microglia) and Ionized calcium-binding adapter molecule 1 (IBA1, red, microglia) in FTD–GRN patient-derived iMGs vs. controls. Nuclei stained with DAPI; scale bar at 10 µm. B Quantification of CD68 intensity in IBA1⁺ iMGs from over 50 cells/experiment in three independent experiments, presented as mean ± SEM. Statistical analysis: ****p < 0.0001, one-way ANOVA, Tukey’s test. C ELISA quantification of sTREM2 in iMGs’ conditioned media (n = 3), shown as means ± SEM; *p < 0.05; one-way ANOVA, Tukey’s test). D Relative mRNA levels of microglia genes (P2RY12, TMEM119, TGFBR1, CX3CR1) in iMGs, normalized to control. Data from three experiments, mean ± SEM; *p < 0.05, **p < 0.01, ***p < 0.001, and ****p < 0.0001; one way ANOVA with post hoc Tukey’s test. E mRNA of pro-inflammatory genes (IL-1β, TNF-α, IL-6) in iMGs, normalized to control. Three experiments, mean ± SEM; *p < 0.05, **p < 0.01, ***p < 0.001, and ****p < 0.0001; one way ANOVA with post hoc Tukey’s test. F Fluorescence images of bead phagocytosis in iMGs; F-actin (green), nuclei (DAPI). Scale bar, 10 µm. G Quantification of phagocytosed beads/iMG cell, over 50 cells/experiment from three independent experiments, mean ± SEM; ****p < 0.0001(ANOVA with post hoc Tukey’s test)