Together, our data suggests that IEC-intrinsic MyD88 triggering can contribute significantly to infection resistance by enforcing the epithelial barrier function, whereas DC-specific MyD88 signaling is critical and sufficient to induce both ILC3 and Th17 cell responses upon infection with C. rodentium. It is thus likely that signals induced by MyD88 triggering in IEC and DC cooperate to induce the full host response during intestinal infections. Here, MYD88 is linked to digestive system infectious disorder.