IL-15 sustains IL-7R-independent ILC2 and ILC3 development.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 28361874.
- Also identified by DOI 10.1038/ncomms14601 and PMC identifier 5380969.
- Licence recorded as CC BY.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
Abstract
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<sup>-/-</sup> mice. Il7ra<sup>-/-</sup> ILC2 primarily express an ST2<sup>-</sup> phenotype, but are not inflammatory ILC2. CCR6<sup>+</sup> ILC3, which express higher Bcl-2 than other ILC3, are the most abundant subset in Il7ra<sup>-/-</sup> 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<sup>-/-</sup> 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.
Medical subject headings
- Interleukin-15
- Lymphocyte Subsets
- Lymphocytes
- Receptors, Interleukin-7