| First Author | Robinette ML | Year | 2017 |
| Journal | Nat Commun | Volume | 8 |
| Pages | 14601 | PubMed ID | 28361874 |
| Mgi Jnum | J:244848 | Mgi Id | MGI:5913627 |
| Doi | 10.1038/ncomms14601 | Citation | Robinette ML, et al. (2017) IL-15 sustains IL-7R-independent ILC2 and ILC3 development. Nat Commun 8:14601 |
| abstractText | The signals that maintain tissue-resident innate lymphoid cells (ILC) in different microenvironments are incompletely understood. Here we show that IL-7 receptor (IL-7R) is not strictly required for the development of any ILC subset, as residual cells persist in the small intestinal lamina propria (siLP) of adult and neonatal Il7ra-/- mice. Il7ra-/- ILC2 primarily express an ST2- phenotype, but are not inflammatory ILC2. CCR6+ ILC3, which express higher Bcl-2 than other ILC3, are the most abundant subset in Il7ra-/- siLP. All ILC subsets are functionally competent in vitro, and are sufficient to provide enhanced protection to infection with C. rodentium. IL-15 equally sustains wild-type and Il7ra-/- ILC survival in vitro and compensates for IL-7R deficiency, as residual ILCs are depleted in mice lacking both molecules. Collectively, these data demonstrate that siLP ILCs are not completely IL-7R dependent, but can persist partially through IL-15 signalling. |
