IFNA16 and tuberculosis: 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).