| First Author | Seo SU | Year | 2015 |
| Journal | Nat Commun | Volume | 6 |
| Pages | 8010 | PubMed ID | 26269452 |
| Mgi Jnum | J:224992 | Mgi Id | MGI:5689944 |
| Doi | 10.1038/ncomms9010 | Citation | Seo SU, et al. (2015) Intestinal macrophages arising from CCR2(+) monocytes control pathogen infection by activating innate lymphoid cells. Nat Commun 6:8010 |
| abstractText | Monocytes play a crucial role in antimicrobial host defence, but the mechanisms by which they protect the host during intestinal infection remains poorly understood. Here we show that depletion of CCR2(+) monocytes results in impaired clearance of the intestinal pathogen Citrobacter rodentium. After infection, the de novo recruited CCR2(+) monocytes give rise to CD11c(+)CD11b(+)F4/80(+)CD103(-) intestinal macrophages (MPs) within the lamina propria. Unlike resident intestinal MPs, de novo differentiated MPs are phenotypically pro-inflammatory and produce robust amounts of IL-1beta (interleukin-1beta) through the non-canonical caspase-11 inflammasome. Intestinal MPs from infected mice elicit the activation of RORgammat(+) group 3 innate lymphoid cells (ILC3) in an IL-1beta-dependent manner. Deletion of IL-1beta in blood monocytes blunts the production of IL-22 by ILC3 and increases the susceptibility to infection. Collectively, these studies highlight a critical role of de novo differentiated monocyte-derived intestinal MPs in ILC3-mediated host defence against intestinal infection. |
