IL-1R8 is highly expressed in the gut epithelium, where it tunes TLR reactivity against commensal bacteria; IL-1R8-deficient mice infected with Citrobacter rodentium displayed an exaggerated IL-1R1 signaling-dependent gut inflammation, causing a severe loss of commensal bacteria and facilitated secondary infection by Salmonella typhimurium [17]. Here, IL1RAPL1 is linked to infection.