| First Author | Coccia M | Year | 2012 |
| Journal | J Exp Med | Volume | 209 |
| Issue | 9 | Pages | 1595-609 |
| PubMed ID | 22891275 | Mgi Jnum | J:190752 |
| Mgi Id | MGI:5449654 | Doi | 10.1084/jem.20111453 |
| Citation | Coccia M, et al. (2012) IL-1beta mediates chronic intestinal inflammation by promoting the accumulation of IL-17A secreting innate lymphoid cells and CD4(+) Th17 cells. J Exp Med 209(9):1595-609 |
| abstractText | Although very high levels of interleukin (IL)-1beta are present in the intestines of patients suffering from inflammatory bowel diseases (IBD), little is known about the contribution of IL-1beta to intestinal pathology. Here, we used two complementary models of chronic intestinal inflammation to address the role of IL-1beta in driving innate and adaptive pathology in the intestine. We show that IL-1beta 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-1beta promotes Th17 responses from CD4(+) T cells and ILCs in the intestine, and we describe synergistic interactions between IL-1beta and IL-23 signals that sustain innate and adaptive inflammatory responses in the gut. These data identify multiple mechanisms through which IL-1beta promotes intestinal pathology and suggest that targeting IL-1beta may represent a useful therapeutic approach in IBD. |
