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

Author

Listed:
  • 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)

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.

Suggested Citation

  • Michelle L. Robinette & Jennifer K. Bando & Wilbur Song & Tyler K. Ulland & Susan Gilfillan & Marco Colonna, 2017. "IL-15 sustains IL-7R-independent ILC2 and ILC3 development," Nature Communications, Nature, vol. 8(1), pages 1-13, April.
    • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_ncomms14601
    DOI: 10.1038/ncomms14601
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    Cited by:

    1. Alberto Díez-Sánchez & Håvard T. Lindholm & Pia M. Vornewald & Jenny Ostrop & Rouan Yao & Andrew B. Single & Anne Marstad & Naveen Parmar & Tovah N. Shaw & Mara Martín-Alonso & Menno J. Oudhoff, 2024. "LSD1 drives intestinal epithelial maturation and controls small intestinal immune cell composition independent of microbiota in a murine model," Nature Communications, Nature, vol. 15(1), pages 1-20, December.

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