Nicotinic acetylcholine receptor agonist attenuates ILC2-dependent airway hyperreactivity

Lauriane Galle-Treger; Yuzo Suzuki; Nisheel Patel; Ishwarya Sankaranarayanan; Jennifer L. Aron; Hadi Maazi; Lin Chen; Omid Akbari

doi:10.1038/ncomms13202

Nature Communications (Oct 2016)

Nicotinic acetylcholine receptor agonist attenuates ILC2-dependent airway hyperreactivity

Lauriane Galle-Treger,
Yuzo Suzuki,
Nisheel Patel,
Ishwarya Sankaranarayanan,
Jennifer L. Aron,
Hadi Maazi,
Lin Chen,
Omid Akbari

Affiliations

Lauriane Galle-Treger: Department of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California
Yuzo Suzuki: Department of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California
Nisheel Patel: Department of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California
Ishwarya Sankaranarayanan: Department of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California
Jennifer L. Aron: Department of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California
Hadi Maazi: Department of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California
Lin Chen: Departments of Biological Science and Chemistry, University of Southern California
Omid Akbari: Department of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California

DOI: https://doi.org/10.1038/ncomms13202
Journal volume & issue: Vol. 7, no. 1
pp. 1 – 13

Abstract

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Airway hyperreactivity is driven by type 2 cytokines produced by ILC2 and Th2 cells. Here the authors show that an α7-nicotinic receptor agonist (GTS-21) inhibits ILC2 responses and is therapeutic against Alternaria-induced airway hyperreactivity in a humanized mouse model.

Published in Nature Communications

ISSN: 2041-1723 (Online)
Publisher: Nature Portfolio
Country of publisher: United Kingdom
LCC subjects: Science
Website: https://www.nature.com/ncomms/

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