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Although very high levels of interleukin (IL)-1β are present in the intestines of patients suffering from inflammatory bowel diseases (IBD), little is known about the contribution of IL-1β to intestinal pathology. Here, we used two complementary models of chronic intestinal inflammation to address the role of IL-1β in driving innate and adaptive pathology in the intestine. We show that IL-1β promotes innate immune pathology in Helicobacter hepaticus-triggered intestinal inflammation by augmenting the recruitment of granulocytes and the accumulation and activation of innate lymphoid cells (ILCs). Using a T cell transfer colitis model, we demonstrate a key role for T cell-specific IL-1 receptor (IL-1R) signals in the accumulation and survival of pathogenic CD4(+) T cells in the colon. Furthermore, we show that IL-1β promotes Th17 responses from CD4(+) T cells and ILCs in the intestine, and we describe synergistic interactions between IL-1β and IL-23 signals that sustain innate and adaptive inflammatory responses in the gut. These data identify multiple mechanisms through which IL-1β promotes intestinal pathology and suggest that targeting IL-1β may represent a useful therapeutic approach in IBD.

Original publication




Journal article


J Exp Med

Publication Date





1595 - 1609


Animals, CD5 Antigens, Cell Survival, Colitis, Colon, Granulocytes, Helicobacter Infections, Helicobacter hepaticus, Immunity, Innate, Interleukin-17, Interleukin-1beta, Interleukin-23, Lymphocytes, Mice, Mice, Inbred C57BL, Receptors, Interleukin-1, Receptors, Interleukin-1 Type I, Th17 Cells