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

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.

SUBMITTER: Robinette ML

PROVIDER: S-EPMC5380969 | biostudies-literature | 2017 Mar

REPOSITORIES: biostudies-literature

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

Robinette Michelle L ML Bando Jennifer K JK Song Wilbur W Ulland Tyler K TK Gilfillan Susan S Colonna Marco M

Nature communications 20170331

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 highe ...[more]

PMID: 28361874

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

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