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. 2024 Jul 18;134(18):e179472. doi: 10.1172/JCI179472

Figure 5. The interaction between FAP+ fibroblasts and CXCL9+ macrophages.

Figure 5

(A) Representative multiplex immunofluorescence (mIF) staining of human fibrotic (right) and nonfibrotic (left) intestinal tissue (original magnification, ×20). DAPI (blue), FAP (red), TWIST1 (green), vimentin (white), CD68 (orange), and CXCL9 (purple) in individual and merged channels are shown. Scale bar: 100 μm. A high-power field (bottom) showing close colocalization between FAP+ fibroblasts (red arrows) and CXCL9+ macrophages (green arrows). The experiment was performed in 4 patients. (B) Quantitative analysis of mIF staining. Proportion of CXCL9+ macrophages to CD68+ cells between fibrotic and nonfibrotic intestinal samples (left); the proportion of CXCL9+ macrophages near to FAP+ fibroblasts (within 30 μm) and far from FAP+ fibroblasts (of 30 μm) per field in fibrosis states (right) was calculated by HALO software (n = 12, 4 patients with 3 fields). Statistical differences were determined by t test. (C) Heatmap showing the activity of the top-ranked ligands inferred to regulate FAP+ fibroblasts by CXCL9+ macrophages according to NicheNet (left), the ligand–receptor interaction between them ordered by ligand activity (middle), and the downstream target genes in FAP+ fibroblasts (right).