Journal
JOURNAL OF EXPERIMENTAL MEDICINE
Volume 209, Issue 9, Pages 1595-1609Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20111453
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Funding
- Wellcome Trust
- Edward Penley Abraham Trust
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Although very high levels of interleukin (IL)-1 beta are present in the intestines of patients suffering from inflammatory bowel diseases (IBD), little is known about the contribution of IL-1 beta to intestinal pathology. Here, we used two complementary models of chronic intestinal inflammation to address the role of IL-1 beta in driving innate and adaptive pathology in the intestine. We show that IL-1 beta 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-1 beta promotes Th17 responses from CD4(+) T cells and ILCs in the intestine, and we describe synergistic interactions between IL-1 beta and IL-23 signals that sustain innate and adaptive inflammatory responses in the gut. These data identify multiple mechanisms through which IL-1 beta promotes intestinal pathology and suggest that targeting IL-1 beta may represent a useful therapeutic approach in IBD.
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