Please use this identifier to cite or link to this item: http://hdl.handle.net/2381/43275
Title: Differential expression of functional chemokine receptors on human blood and lung group 2 innate lymphoid cells.
Authors: Weston, CA
Rana, BMJ
Cousins, DJ
First Published: 8-Sep-2018
Publisher: Elsevier for American Academy of Allergy, Asthma and Immunology, Mosby
Citation: Journal of Allergy and Clinical Immunology, 2019, 143(1), pp. 410-413.e9
Abstract: [First paragraph] Innate lymphoid cells (ILCs), primarily found at mucosal barriers, provide immediate protection against the establishment and spread of infection. ILCs have been divided into 3 subsets analogous to TH cells1: ILC1, ILC2, and ILC3. ILC2s are similar to TH2 cells and express IL-4, IL-5, and IL-13 and were initially identified as a non–T-, non–B-cell source of type 2 cytokines.2 They are found in the blood, gut, skin, and lung where they contribute to host defence. Upon activation, ILCs rapidly produce a large quantity of cytokines and other mediators, which attract and activate other inflammatory cells. In various models of airway disease, ILC2 numbers have been shown to increase with allergen challenge, leading to a significant increase in type 2 inflammatory cytokines.3 Recent studies have demonstrated the existence of a complex interplay between lung epithelial cells and ILC2s that is required for asthma persistence in a mouse model. Furthermore, human studies have suggested that ILC2s provide the key link between viral infection and airway inflammation leading to asthma exacerbations.
DOI Link: 10.1016/j.jaci.2018.08.030
eISSN: 1097-6825
Links: https://www.sciencedirect.com/science/article/pii/S0091674918312764?via%3Dihub
http://hdl.handle.net/2381/43275
Version: Publisher Version
Status: Peer-reviewed
Type: Journal Article
Rights: Copyright © the authors, 2018. This is an open-access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Appears in Collections:Published Articles, Dept. of Infection, Immunity and Inflammation

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