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). The gene discussed is IFNGR2; the disease is bacterial urinary tract infection.