The Role of ILC2s in Asthma Pathogenesis

Description

This template was adapted from the original submission. Edits were made to enhance scientific accuracy, optimal usability and/or to meet industry-leading design standards for science communication. Allergens, viruses or helminths can provoke the release of alarmins from the damaged epithelium. These stimulate the GATA3+/RORa+ ILC2s to express type 2 cytokines. Interleukins-4, -5 and -13 can cause IgE increase from plasma cells, eosinophil expansion, and airway hyper-responsiveness, respectively. Alternatively, through an unknown mechanism, alarmins can mildly stimulate ILC2s to secrete amphiregulin in order to repair the damaged epithelial cells.

Acknowledgements

References

Monticelli, L.A., et al.. (2011) Innate lymphoid cells promote lung-tissue homeostasis after infection with influenza virus.. Nature Immunology. https://doi.org/10.1038/ni.2131 Klein Wolterink, R.G., et al.. (2012) Pulmonary innate lymphoid cells are major producers of IL-5 and IL-13 in murine models of allergic asthma.. Eur J Immunol. https://doi.org/10.1002/eji.201142018 Camelo, A., et al.. (2017) IL-33, IL-25, and TSLP induce a distinct phenotypic and activation profile in human type 2 innate lymphoid cells.. Blood advances. https://doi.org/10.1182/bloodadvances.2016002352

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