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Nat Commun. 2019 May 14;10(1):2162. doi: 10.1038/s41467-019-09883-7.

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

Author information

1
Department of Experimental Immunology, Amsterdam UMC, University of Amsterdam, Location AMC, Meibergdreef 9, Amsterdam, 1105, AZ, The Netherlands.
2
Department of Immunology and Microbiology, Lab of Clinical Immunology, KU Leuven, Belgium Herestraat 49-box 1030, BE-3000, Leuven, Belgium.
3
Department of Otorhinolaryngology, Amsterdam UMC, University of Amsterdam, Location AMC, Meibergdreef 9, Amsterdam, 1105, AZ, The Netherlands.
4
Department of Experimental Immunology, Amsterdam UMC, University of Amsterdam, Location AMC, Meibergdreef 9, Amsterdam, 1105, AZ, The Netherlands. hergen.spits@amc.uva.nl.

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.

PMID:
31089134
PMCID:
PMC6517442
DOI:
10.1038/s41467-019-09883-7
[Indexed for MEDLINE]
Free PMC Article

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