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

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. Drunen, Wytske J. Fokkens, Hergen Spits () and Suzanne M. Bal
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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

Nature Communications, 2019, vol. 10, issue 1, 1-15

Abstract: 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.

Date: 2019
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DOI: 10.1038/s41467-019-09883-7

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