The airway epithelium in asthma.
Airway epithelium
Alarmins
Asthma
Endoplasmic reticulum stress
Endotype
IL-13
IL-17
Interferon
Mucus
Type 2-high asthma
Journal
Advances in immunology
ISSN: 1557-8445
Titre abrégé: Adv Immunol
Pays: United States
ID NLM: 0370425
Informations de publication
Date de publication:
2019
2019
Historique:
entrez:
13
7
2019
pubmed:
13
7
2019
medline:
16
4
2020
Statut:
ppublish
Résumé
Asthma is a genetically and phenotypically complex disease that has a major impact on global health. Signs and symptoms of asthma are caused by the obstruction of airflow through the airways. The epithelium that lines the airways plays a major role in maintaining airway patency and in host defense. The epithelium initiates responses to inhaled or aspirated substances, including allergens, viruses, and bacteria, and epithelial-derived cytokines are important in the recruitment and activation of immune cells in the airway. Changes in the structure and function of the airway epithelium are a prominent feature of asthma. Approximately half of individuals with asthma have evidence of active type 2 immune responses in the airway. In these individuals, epithelial cytokines promote type 2 responses, and responses to type 2 cytokines result in increased epithelial mucus production and other effects that cause airway obstruction. Recent work also implicates other epithelial responses, including interleukin-17, interferon and ER stress responses, that may contribute to asthma pathogenesis and provide new targets for therapy.
Identifiants
pubmed: 31296301
pii: S0065-2776(19)30015-X
doi: 10.1016/bs.ai.2019.05.001
pii:
doi:
Substances chimiques
Alarmins
0
Allergens
0
Interleukin-13
0
Interleukin-17
0
Interferons
9008-11-1
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
1-34Subventions
Organisme : NHLBI NIH HHS
ID : R35 HL145235
Pays : United States
Organisme : NIAID NIH HHS
ID : U19 AI077439
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL138424
Pays : United States
Informations de copyright
© 2019 Elsevier Inc. All rights reserved.