Neonatal HSCs are resistant to inflammation-induced acute Mk lineage differentiation. (A) pIpC challenge in 10-day-old (d10) and adult mice. (B-C) Representative FACS data showing BM HSCs for experiment outlined in panel A. (D) CD41⁺ HSC frequency in PBS- or pIpC-treated mice of the indicated ages (n = 6-9 for each treatment/age). Error bars indicate standard deviation of the mean. Statistical significance determined by multiple t tests using the Holm-Šídák method. (E) Representative merged UMAP visualization of concatenated FACS data from d10 and ABM HSPCs 16 hours after pIpC (purple) or PBS (black) treatment. (F) Gene set enrichment analysis of the interferon-α (IFN-α) response hallmark gene set.⁶⁶ (G) Relative accessibility for select IFN-inducible genes represented as the fraction of single cells with detectable ATAC-seq signal. (H) FACS analysis of 12-week-old (12w) Ifnar-deficient mice. Upper panel: CD41⁺ frequency in HSCs of the indicated genotypes (n = 4-12). Lower panel: representative histogram overlay of CD41 expression. (I) FACS analysis of 2-day-old (d2) Ifnar-deficient pups. Upper panel: CD41⁺ frequency in HSCs of the indicated genotypes (n = 4-11). Lower panel: representative histogram overlay of CD41 expression. Statistical significance was determined by using the Kruskal-Wallis test followed by Dunn’s multiple comparisons test. EPCR, endothelial protein C receptor; FDR, false discovery rate; LSK, lineage^–Sca1⁺cKit⁺; NES, normalized enrichment score.