Extended Data Fig. 3: scRNA-seq analysis of lungs from mice exposed to cigarette smoke and treated with LTβR–Ig.
From: Inhibition of LTβR signalling activates WNT-induced regeneration in lung
Cells from whole lung suspensions of B6 mice exposed to filtered air (n = 3) or cigarette smoke for 6 months, plus LTβR–Ig fusion protein (n = 5) or control Ig (n = 5) therapeutically from 4 to 6 months, were analysed at 6 months by scRNA-seq (Drop-Seq). a, Heat map depicting the expression of key genes used in identifying the individual cell populations. b, UMAP of scRNA-seq profiles (dots) coloured by experimental group. c, UMAP plots showing expression of genes indicated in scRNA-seq profiles. d, Dot blot depicting the expression level (log-transformed, normalized UMI counts) and percentage of cells in a population positive for Ltb, Lta, Tnf, Tnfsf14, Ltbr, Tnfrsf1a and Tnfrsf1b. e, UMAP plot showing the relative intensity of the positive regulation of NIK (non-canonical) NF-κB signalling pathway (GO:1901224) across the scRNA-seq profiles. f, UMAP plot of scRNA-seq profiles (dots) of lung epithelial cells coloured by experimental group (left) and the relative intensity of the positive regulation of NIK (non-canonical) NF-κB signalling pathway (GO:1901224) (right). g, Box and whiskers plot (box representing 25th–75th percentile, median line indicated and Tukey whiskers representing ± 1.5× IQR) showing the relative score for the positive regulation of NIK (non-canonical) NF-κB signalling pathway in the cell types indicated across the three groups. Statistical significance was assessed using Wilcoxon rank-sum two-sided test on normalized, log-transformed count values and corrected with Benjamini–Hochberg.
