Cytokine and Lipid Mediator Regulation of Group 2 Innate Lymphoid Cells (ILC2s) in Human Allergic Airway Disease
Kellen Cavagnero and Taylor A. Doherty*
Department of Medicine, University of California San Diego, USA
- *Corresponding Author:
- Taylor A. Doherty
Department of Medicine, University of California San Diego, Biomedical Sciences Building
Room 5090, 9500 Gilman Drive, La Jolla, CA 92093-0635, USA
Tel: (858) 822-7653
Fax: (858) 534-2110
E-mail: [email protected]
Received date: July 18, 2017; Accepted date: July 26, 2017; Published date: August 04, 2017
Citation: Cavagnero K, Doherty TA (2017) Cytokine and Lipid Mediator Regulation of Group 2 Innate Lymphoid Cells (ILC2s) in Human Allergic Airway Disease. J Cytokine Biol 2:116.
Copyright: © 2017 Cavagnero K, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
The recent discovery of group 2 innate lymphoid cells (ILC2s) has caused a paradigm shift in the understanding of allergic airway disease pathogenesis. Prior to the discovery of ILC2s, Th2 cells were largely thought to be the primary source of type 2 cytokines; however, activated ILC2s have since been shown to contribute significantly, and in some cases, dominantly to type 2 cytokine production. Since the discovery of ILC2s in 2010, many mediators have been shown to regulate their effector functions. Initial studies identified the epithelial derived cytokines IL-25, IL-33, and TSLP as activators of ILC2s, and recent studies have identified many additional cytokine and lipid mediators that are involved in ILC2 regulation. ILC2s and their mediators represent novel therapeutic targets for allergic airway diseases and intensive investigation is underway to better understand ILC2 biology and upstream and downstream pathways that lead to ILC2-driven airway pathology. In this review, we will focus on the cytokine and lipid mediators that regulate ILC2s in human allergic airway disease, as well as highlight newly discovered mediators of mouse ILC2s that may eventually translate to humans.