IL1RL2 and colitis: Induction of IL-36 receptor signaling through any one of its ligands, IL-36α, IL-36β, or IL-36γ, induced proliferation of intestinal epithelial cells in in vitro organoid cultures, and mice with genetic deletion of the IL-36 receptor were more susceptible to chemically induced colitis, demonstrating higher disease activity, more severe colon pathology, greater bacterial translocation, and decreased survival.