• Patrick D Mitchell and Paul M O'Byrne.
• Firestone Institute of Respiratory Health and the Department of Medicine, Michael G DeGroote School of Medicine, McMaster University, Hamilton, ON, Canada.
• Chest. 2017 Jun 1; 151 (6): 133813441338-1344.

AbstractThe interaction between the airway epithelium and the inhaled environment is crucial to understanding the pathobiology of asthma. Several studies have identified an important role of airway epithelial-derived cytokines, IL-25, IL-33, and thymic stromal lymphopoietin (TSLP) in asthma pathogenesis. These cytokines have been described as epithelial-derived alarmins that activate and potentiate the innate and humoral arms of the immune system in the presence of actual or perceived damage. Each of the three epithelial-derived alarmins has been implicated in the pathobiology of inhaled allergen-induced airway responses. The best evidence to date exists for TSLP, in that a human monoclonal antibody, which binds TSLP and prevents its engagement with its receptor, resolves airway inflammation in patients with allergic asthma and attenuates allergen-induced airway responses. Better understanding the roles that the epithelial-derived alarmins play and how they influence airway immune response may allow the development of novel therapeutics for asthma treatment.Copyright © 2016 American College of Chest Physicians. Published by Elsevier Inc. All rights reserved.

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