| First Author | Bando JK | Year | 2018 |
| Journal | Immunity | Volume | 48 |
| Issue | 6 | Pages | 1208-1219.e4 |
| PubMed ID | 29858011 | Mgi Jnum | J:267632 |
| Mgi Id | MGI:6268897 | Doi | 10.1016/j.immuni.2018.04.012 |
| Citation | Bando JK, et al. (2018) The Tumor Necrosis Factor Superfamily Member RANKL Suppresses Effector Cytokine Production in Group 3 Innate Lymphoid Cells. Immunity 48(6):1208-1219.e4 |
| abstractText | While signals that activate group 3 innate lymphoid cells (ILC3s) have been described, the factors that negatively regulate these cells are less well understood. Here we found that the tumor necrosis factor (TNF) superfamily member receptor activator of nuclear factor kappaB ligand (RANKL) suppressed ILC3 activity in the intestine. Deletion of RANKL in ILC3s and T cells increased C-C motif chemokine receptor 6 (CCR6)(+) ILC3 abundance and enhanced production of interleukin-17A (IL-17A) and IL-22 in response to IL-23 and during infection with the enteric murine pathogen Citrobacter rodentium. Additionally, CCR6(+) ILC3s produced higher amounts of the master transcriptional regulator RORgammat at steady state in the absence of RANKL. RANKL-mediated suppression was independent of T cells, and instead occurred via interactions between CCR6(+) ILC3s that expressed both RANKL and its receptor, RANK. Thus, RANK-RANKL interactions between ILC3s regulate ILC3 abundance and activation, suggesting that cell clustering may control ILC3 activity. |
