Notably, IFNG-IFNGR2-mediated interactions between ILC3s and monocytes and macrophages were significantly increased in the context of UTI, and specific to ILC3s (Figure 7G), consistent with the decrease in Interferon gamma response pathway genes we observed in ILC-depleted Rag2 mice (Figure 5I). This evidence concerns the gene IFNG and bacterial urinary tract infection.