IL-15 sustains IL-7R-independent ILC2 and ILC3 development

Michelle L. Robinette, Jennifer K. Bando, Wilbur Song, Tyler K. Ulland, Susan Gilfillan and Marco Colonna ()
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Michelle L. Robinette: Washington University School of Medicine
Jennifer K. Bando: Washington University School of Medicine
Wilbur Song: Washington University School of Medicine
Tyler K. Ulland: Washington University School of Medicine
Susan Gilfillan: Washington University School of Medicine
Marco Colonna: Washington University School of Medicine

Nature Communications, 2017, vol. 8, issue 1, 1-13

Abstract: 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.

Date: 2017
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DOI: 10.1038/ncomms14601

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