Fig. 3: Immunofibroblasts and CCL21 CCL19 pericytes show differential dependence on signalling pathways.

a Select pathways from the gene-set overrepresentation analysis (using GO and Kegg gene sets) of fibroblast and mural populations highlighting the enrichment of interferon and TNF pathways in both immunofibroblasts and CCL21 CCL19 pericytes, and NFκB pathway enrichment restricted to immunofibroblasts. b Violin plot of expression of genes related to the enriched pathways shown in Fig. 3a across fibroblast and mural clusters. c Multiplex immunofluorescence image of ccl21rna (green), ccl19rna (red) vascular expression in DAPI (blue) and CD45⁺ (yellow) immune aggregate in TLS-induced salivary glands of wildtype (wt) and lymphotoxin beta receptor knockout (Ltbr^–/–) mice, n = 2 per group, Scale bar = 100 µm. Ltbr^–/– results in abrogation of TLS and decreased CCL19 expression within immune aggregates. Perivascular expression of CCL19 remained in the Ltβr^–/–. d Flow cytometric analysis of TLS-induced salivary glands of wildtype (wt) and Ltbr^–/– mice for CCL21+CD34+ immunofibroblast and CCL21⁺CD146⁺ pericytes to confirm the dependence of immunofibroblasts on LTβR signalling and CCL21 CCL19 pericyte independence. Data are mean ± s.e.m from two independent experiments with two mice analyzed per group. Number of asterisks indicate significance: *p < 0.05, Mann–Whitney test, two-tailed. e Clustering of cell type by SCENIC derived regulon activity displaying distinct clustering of the fibroblast and mural lineages. f Heatmap of the regulon activity of the top 15 regulons by activity for the fibroblast CCL19 TNFSF13B and the pericyte CCL21 CCL19 clusters.