| First Author | Galle-Treger L | Year | 2016 |
| Journal | Nat Commun | Volume | 7 |
| Pages | 13202 | PubMed ID | 27752043 |
| Mgi Jnum | J:242598 | Mgi Id | MGI:5905708 |
| Doi | 10.1038/ncomms13202 | Citation | Galle-Treger L, et al. (2016) Nicotinic acetylcholine receptor agonist attenuates ILC2-dependent airway hyperreactivity. Nat Commun 7:13202 |
| abstractText | Allergic asthma is a complex and chronic inflammatory disorder that is associated with airway hyperreactivity (AHR) and driven by Th2 cytokine secretion. Type 2 innate lymphoid cells (ILC2s) produce large amounts of Th2 cytokines and contribute to the development of AHR. Here, we show that ILC2s express the alpha7-nicotinic acetylcholine receptor (alpha7nAChR), which is thought to have an anti-inflammatory role in several inflammatory diseases. We show that engagement of a specific agonist with alpha7nAChR on ILC2s reduces ILC2 effector function and represses ILC2-dependent AHR, while decreasing expression of ILC2 key transcription factor GATA-3 and critical inflammatory modulator NF-kappaB, and reducing phosphorylation of upstream kinase IKKalpha/beta. Additionally, the specific alpha7nAChR agonist reduces cytokine production and AHR in a humanized ILC2 mouse model. Collectively, our data suggest that alpha7nAChR expressed by ILC2s is a potential therapeutic target for the treatment of ILC2-mediated asthma. |
