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IL-1β, IL-23, and TGF-β drive plasticity of human ILC2s towards IL-17-producing ILCs in nasal inflammation. 2019
Korneliusz Golebski, and
Xavier R Ros, and
Maho Nagasawa, and
Sophie van Tol, and
Balthasar A Heesters, and
Hajar Aglmous, and
Chantal M A Kradolfer, and
Medya M Shikhagaie, and
Sven Seys, and
P W Hellings, and
Cornelis M van Drunen, and
Wytske J Fokkens, and
Hergen Spits, and
Suzanne M Bal
Department of Experimental Immunology, Amsterdam UMC, University of Amsterdam, Location AMC, Meibergdreef 9, Amsterdam, 1105, AZ, The Netherlands.
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.
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