In addition, mice with a specific IL-10Rα deletion in macrophages developed no spontaneous colitis in a Helicobacter negative facility, but exhibited enhanced susceptibility to transfer colitis and DSS-induced colitis, which was associated with elevated production of TNFα and IL-1β by IL-10Rα-deficient macrophages, leading to enhanced Th17 responses [34, 35]. Here, IL10RA is linked to colitis.