Relative to IgG lesions, naive cell-cell interaction networks were dominated by signaling from neutrophils, macrophages, and non-immune cells (endothelial cells and fibroblasts) and enriched for type 1 immune (CXCL9–11, IL6 IL1B, TNF) and type 1 IFN (IFNB1, IFNA1, IFNA2, IFNA16)57 signaling—the latter implicated in TB pathogenesis and previously demonstrated to contribute to neutrophil extracellular trap formation and subsequent Mtb proliferation (Figures 7A, 7B, and S5A–S5E). This evidence concerns the gene IFNA1 and tuberculosis.