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IL-15 Sustains IL-7R-independent ILC2 and ILC3 Development

Overview
Journal Nat Commun
Specialty Biology
Date 2017 Apr 1
PMID 28361874
Citations 66
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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 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.

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