| First Author | Muzaki AR | Year | 2016 |
| Journal | Mucosal Immunol | Volume | 9 |
| Issue | 2 | Pages | 336-51 |
| PubMed ID | 26174764 | Mgi Jnum | J:279213 |
| Mgi Id | MGI:6356500 | Doi | 10.1038/mi.2015.64 |
| Citation | Muzaki AR, et al. (2016) Intestinal CD103(+)CD11b(-) dendritic cells restrain colitis via IFN-gamma-induced anti-inflammatory response in epithelial cells. Mucosal Immunol 9(2):336-51 |
| abstractText | A crosstalk between commensals, gut immune cells, and colonic epithelia is required for a proper function of intestinal mucosal barrier. Here we investigated the importance of two distinct intestinal dendritic cell (DC) subsets in controlling intestinal inflammation. We show that Clec9A-diphtheria toxin receptor (DTR) mice after depletion of CD103(+)CD11b(-) DCs developed severe, low-dose dextran sodium sulfate (DSS)-induced colitis, whereas the lack of CD103(+)CD11b(+) DCs in Clec4a4-DTR mice did not exacerbate intestinal inflammation. The CD103(+)CD11b(-) DC subset has gained a functional specialization that able them to repress inflammation via several epithelial interferon-gamma (IFN-gamma)-induced proteins. Among others, we identified that epithelial IDO1 and interleukin-18-binding protein (IL-18bp) were strongly modulated by CD103(+)CD11b(-) DCs. Through its preferential property to express IL-12 and IL-15, this particular DC subset can induce lymphocytes in colonic lamina propria and in epithelia to secrete IFN-gamma that then can trigger a reversible early anti-inflammatory response in intestinal epithelial cells. |
