A team of scientists at the Wellcome Trust Sanger Institute recently identified the IL-22 receptor Il22ra1 as a new factor that protects human intestine against opportunistic pathogens, such as the bacteria Enterococcus faecalis. Their findings were published in September issue of Cell Host and Microbe in a study entitled, “Epithelial IL-22RA1-mediated fucosylation promotes colonization resistance to an opportunistic pathogen.” IL-22, important for homeostasis in mucosal barriers, including the gastrointestinal tract, was previously associated with pathological interactions between host and microbiota. However, IL-22's effects on resistance/susceptibility to pathogens' colonization were recognized to depend both on native microbiota and inflammatory host statues. In this study, the authors observed that when deleting the gene coding for the IL-22 receptor in mice, Il22ra1 was associated with disruption of the indigenous microbiota, leading to Enterococcus faecalis bacteria dissemination. Microbiota disruption was achieved by infecting mice with Citrobacter rodentium or by chemical-induced colitis. Notably, in humans, Il22ra1 isassociated with Inflammatory Bowel Disease (IBD).