| First Author | Rahabi M | Year | 2020 |
| Journal | Cell Rep | Volume | 30 |
| Issue | 13 | Pages | 4386-4398.e5 |
| PubMed ID | 32234475 | Mgi Jnum | J:287654 |
| Mgi Id | MGI:6416770 | Doi | 10.1016/j.celrep.2020.03.018 |
| Citation | Rahabi M, et al. (2020) Divergent Roles for Macrophage C-type Lectin Receptors, Dectin-1 and Mannose Receptors, in the Intestinal Inflammatory Response. Cell Rep 30(13):4386-4398.e5 |
| abstractText | Colonic macrophages are considered to be major effectors of inflammatory bowel diseases (IBDs) and the control of gut inflammation through C-type lectin receptors is an emerging concept. We show that during colitis, the loss of dectin-1 on myeloid cells prevents intestinal inflammation, while the lack of mannose receptor (MR) exacerbates it. A marked increase in dectin-1 expression in dextran sulfate sodium (DSS)-exposed MR-deficient mice supports the critical contribution of dectin-1 to colitis outcome. Dectin-1 is crucial for Ly6C(high)CCR2(high) monocyte population enrichment in the blood and their recruitment to inflamed colon as precursors of inflammatory macrophages. Dectin-1 also promotes inflammasome-dependent interleukin-1beta (IL-1beta) secretion through leukotriene B4 production. Interestingly, colonic inflammation is associated with a concomitant overexpression of dectin-1/CCL2/LTA4H and downregulation of MR on macrophages from IBD patients. Thus, MR and dectin-1 on macrophages are important mucosal inflammatory regulators that contribute to the intestinal inflammation. |
