Fig. 3

FSTL1 facilitates stem cell-mediated Ly6C−CX3CR1+ subset remodelling. a UMAP analysis of 4300 macrophages from 3 PBS- and 3 MSC-treated mice identified 15 distinct cell clusters. b Cluster distribution of cells in PBS- (gray) and MSC- (purple) treated mice. c Comparison of the populations of different cell lineages between PBS-treated and MSC-treated livers. d The relative percentages of different cell lineages in each group, coloured according to cell lineage. PBS: n = 3 liver samples from PBS-treated mice; MSC: n = 3 liver samples from MSC-treated mice. e Heatmap displaying the relative expression levels of marker genes in 15 cell lineages (top, colour-coded by cell lineage), with exemplar genes labelled in Cluster 5. The columns denote cells; the rows denote genes. f Marker expression in different clusters. g–j The percentages of the Ly6C−CX3CR1+ subset among the total viable hepatic CD45+ cells and the cell count of the Ly6C−CX3CR1+ subset were normalized to the liver weight, as determined by flow cytometry. g, h The Ly6C−CX3CR1+ subset was evaluated in Fstl1+/− (n = 6) and WT littermates (n = 6) at 24 h (g) and 48 h (h) after MSC infusion. i The Ly6C−CX3CR1+ subset was evaluated in C57BL/6 mice treated with (n = 5) or without the FSTL1 neutralizing antibody 22B6 (n = 5) at 48 h after MSC infusion. j The Ly6C−CX3CR1+ subset was evaluated in Fstl1+/− (n = 5) and WT littermates (n = 5) at 48 h after MNC infusion. *p < 0.05, **p < 0.01, ***p < 0.001, and n.s., not significant. Statistical significance was determined by a two-tailed unpaired t-test (g–j). Data are presented as the mean ± SEM and were pooled from at least three independent experiments