Fig. 1: Characterization of human iMGLs derived from monozygotic twins discordant for SCZ.
From: Genetic contribution to microglial activation in schizophrenia
a Timeline for iMGL differentiation. Scale bar 50 µm in all. Generated iMGLs expressed (b) on protein level pan-macrophage marker IBA1, and microglia-specific markers P2Y12, TREM2 and CX3CR1 (nuclei on blue, scale bar 50 µm), and (c) on transcriptomic level AIF1 (IBA1; H(3) = 10.08, p = 0.0035), ITGAM (CD11b; H(3) = 10.93, p = 0.001; HPC vs. iMGL U = 0, p = 0.0286; iMGL vs. iMGL + LPS U = 0, p = 0.0286), P2RY12 (H(3) = 8.717, p = 0.014; HPC vs. iMGL U = 0, p = 0.0286; iMGL vs. iMGL + LPS U = 0, p = 0.0286) and TREM2 (H(3) = 9.175, p = 0.009; HPC vs. iMGL U = 0, p = 0.0286; iMGL vs. iMGL + LPS U = 0, p = 0.0286). Kruskal–Wallis test, Mann–Whitney test, n = 3–4 CTRL lines. d Illustration of patient cohort created with BioRender. e RNA expression of AIF1, TREM2, PTPRC (CD45) and TMEM119 based on bulk RNA sequencing. CTRL healthy individuals, ST affected twin, HT healthy twin, HPC hematopoietic stem cell, iMφ hiPSC-macrophage, iMGL hiPSC-microglia like cell, iMGL + LPS LPS-treated iMGL.
