A study by Friedrich et al. [48] reported that during intestinal infection, functional MyD88 signaling (downstream signal of TLR5) in CD11c+ cells was sufficient to activate intestinal DCs, induce TH cell development, generate enhanced epithelial barrier integrity, and increase expression of the antimicrobial peptide RegIIIγ by epithelial cells, which was consistent with our findings. This evidence concerns the gene MYD88 and digestive system infectious disorder.