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IL-1β, IL-23, and TGF-β drive plasticity of human ILC2s towards IL-17-producing ILCs in nasal inflammation

Author

Listed:
  • Korneliusz Golebski

    (University of Amsterdam)

  • Xavier R. Ros

    (University of Amsterdam)

  • Maho Nagasawa

    (University of Amsterdam)

  • Sophie Tol

    (University of Amsterdam)

  • Balthasar A. Heesters

    (University of Amsterdam)

  • Hajar Aglmous

    (University of Amsterdam)

  • Chantal M. A. Kradolfer

    (University of Amsterdam)

  • Medya M. Shikhagaie

    (University of Amsterdam)

  • Sven Seys

    (KU Leuven)

  • P. W. Hellings

    (KU Leuven)

  • Cornelis M. Drunen

    (University of Amsterdam)

  • Wytske J. Fokkens

    (University of Amsterdam)

  • Hergen Spits

    (University of Amsterdam)

  • Suzanne M. Bal

    (University of Amsterdam)

Abstract

Innate lymphoid cells (ILCs) are crucial for the immune surveillance at mucosal sites. ILCs coordinate early eradication of pathogens and contribute to tissue healing and remodeling, features that are dysfunctional in patients with cystic fibrosis (CF). The mechanisms by which ILCs contribute to CF-immunopathology are ill-defined. Here, we show that group 2 ILCs (ILC2s) transdifferentiated into IL-17-secreting cells in the presence of the epithelial-derived cytokines IL-1β, IL-23 and TGF-β. This conversion is abrogated by IL-4 or vitamin D3. IL-17 producing ILC2s induce IL-8 secretion by epithelial cells and their presence in nasal polyps of CF patients is associated with neutrophilia. Our data suggest that ILC2s undergo transdifferentiation in CF nasal polyps in response to local cytokines, which are induced by infectious agents.

Suggested Citation

  • Korneliusz Golebski & Xavier R. Ros & Maho Nagasawa & Sophie Tol & Balthasar A. Heesters & Hajar Aglmous & Chantal M. A. Kradolfer & Medya M. Shikhagaie & Sven Seys & P. W. Hellings & Cornelis M. Drun, 2019. "IL-1β, IL-23, and TGF-β drive plasticity of human ILC2s towards IL-17-producing ILCs in nasal inflammation," Nature Communications, Nature, vol. 10(1), pages 1-15, December.
    • Handle: RePEc:nat:natcom:v:10:y:2019:i:1:d:10.1038_s41467-019-09883-7
    DOI: 10.1038/s41467-019-09883-7
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