Journal
CHEST
Volume 151, Issue 6, Pages 1338-1344Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.chest.2016.10.042
Keywords
airway inflammation; asthma; cytokines
Categories
Funding
- AstraZeneca
- Chiesi
- Novartis
- Boehringer Ingelheim
- GSK
- MedImmune
- Merck
- Abbott
- Amgen
- Genentech
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The 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.
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