| First Author | Manta C | Year | 2013 |
| Journal | Mucosal Immunol | Volume | 6 |
| Issue | 1 | Pages | 177-88 |
| PubMed ID | 22854708 | Mgi Jnum | J:315488 |
| Mgi Id | MGI:6829062 | Doi | 10.1038/mi.2012.61 |
| Citation | Manta C, et al. (2013) CX(3)CR1(+) macrophages support IL-22 production by innate lymphoid cells during infection with Citrobacter rodentium. Mucosal Immunol 6(1):177-88 |
| abstractText | Innate immune cells, such as intestinal epithelial cells, dendritic cells (DCs), macrophages, granulocytes, and innate lymphoid cells provide a first line of defence to enteric pathogens. To study the role of CX(3)CR1(+) DCs and macrophages in host defence, we infected CX(3)CR1-GFP animals with Citrobacter rodentium. When transgenic CX(3)CR1-GFP animals are infected with the natural mouse pathogen C. rodentium, CX(3)CR1(-/-) animals showed a delayed clearance of C. rodentium as compared with (age- and sex-matched) wild-type B6 animals. The delayed clearance of C. rodentium is associated with reduced interleukin (IL)-22 expression. In C. rodentium-infected CX(3)CR1-GFP animals, IL-22 producing lymphoid-tissue inducer cells (LTi cells) were selectively reduced in the absence of CX(3)CR1. The reduced IL-22 expression correlates with decreased expression of the antimicrobial peptides RegIIIbeta and RegIIIgamma. The depletion of CX(3)CR1(+) cells by diphtheria toxin injection in CX(3)CR1-GFP x CD11c.DOG animals confirmed the role of CX(3)CR1(+) phagocytes in establishing IL-22 production, supporting the clearance of a C. rodentium infection. |
