Fig. 4: Mapping the immune–epithelial cell interactions in glomerular crescent formation.

a, Circle plot showing cell–cell interactions in cGN compared to control samples. The interaction edges are colored the same as the source cell type whereas edge weights are proportional to the interaction strength. b, Heatmap showing the signaling pathways that have increased activity directed toward PECs in cGN and the source cell types producing the corresponding ligands, colored by the interaction probability. c, Scores for PDGF and TGFβ pathway activation in PECs plotted along pseudotime (lines show quadratic regression fits with 95% confidence intervals). d, Schematic representation of the PDGF signaling pathway, highlighting the genes upregulated in PECs in an snRNA-seq dataset from samples from patients with ANCA-GN (n = 11) over controls (n = 4). e, Multiplexed protein staining on a Xenium slide showing overexpression of Ki-67 in cGN samples (representative images of eight samples: two control (top left), three ANCA-GN (bottom left), two SLE (top right) and one anti-GBM disease (bottom right); representative of two independent experiments). f, Expression of Ki-67 protein in PECs along PC1. The primary axis corresponds to fluorescence intensity values of Ki-67. The secondary axis curve shows the change in percentage of Ki-67-positive cells per glomerulus. g, Schematic representation of the TGFβ signaling pathway, highlighting the genes from this pathway upregulated in PECs in an snRNA-seq dataset from samples from patients with ANCA-GN (n = 11) over controls (n = 4). h, Scatter plot showing correlation of TGFβ pathway score with fibrosis score in PECs (top) and the patient median TGFβ pathway score to the individual kidney function (bottom) (Spearman’s correlation, two-sided). i, Schematic illustrating the role of PDGF-mediated and TGFβ-mediated activation of PECs in crescent formation and glomerulosclerosis in cGN.