Interleukin 1β Mediates Intestinal Inflammation in Mice and Patients With Interleukin 10 Receptor Deficiency.

ABSTRACT: Interleukin 10 receptor (IL10R)-deficient mice develop spontaneous colitis and, similarly, patients with loss-of-function mutations in IL10R develop severe infant-onset inflammatory bowel disease. Loss of IL10R signaling in mouse and human macrophages is associated with increased production of interleukin 1β. We demonstrated that innate immune production of IL1β mediates colitis in IL10R-deficient mice. Transfer of Il1r1^-/- CD4⁺ T cells into Rag1^-/-/Il10rb^-/- mice reduced the severity of their colitis (compared to mice that received CD4⁺ T cells that express IL1R), accompanied by decreased production of interferon gamma, tumor necrosis factor-α, and IL17A. In macrophages from mice without disruption of IL10R signaling or from healthy h

SUBMITTER: Shouval DS 

PROVIDER: S-EPMC5124405 | biostudies-literature | 2016 Dec

REPOSITORIES: biostudies-literature