Friday, 16 October 2015: 11:45 - 12:05
Grand Ballroom 104 (Coex Convention Center)
Learning Objectives:
Due to the heterogeneity of severe asthma, there is no “standard” treatment and individualized treatment is mandatory. Unsupervised cluster analysis has identified several clinical phenotypes such as early-onset allergic asthma, later-onset obese asthma, later-onset eosinophilic asthma, etc. Furthermore, molecular phenotyping, based on the gene expression profiles in the airways or blood cells, has identified Th2-high/low phenotypes with different levels of serum periostin. In the present symposium, I will first discuss the similarities and differences between “periostin-high” and “eosinophilic” phenotypes of severe asthma. Secondly, I will present a possible mechanism of corticosteroid-insensitivity in “innate-type allergy” induced by group 2 innate lymphoid cells (ILC2s).
Due to the heterogeneity of severe asthma, there is no “standard” treatment and individualized treatment is mandatory. Unsupervised cluster analysis has identified several clinical phenotypes such as early-onset allergic asthma, later-onset obese asthma, later-onset eosinophilic asthma, etc. Furthermore, molecular phenotyping, based on the gene expression profiles in the airways or blood cells, has identified Th2-high/low phenotypes with different levels of serum periostin. In the present symposium, I will first discuss the similarities and differences between “periostin-high” and “eosinophilic” phenotypes of severe asthma. Secondly, I will present a possible mechanism of corticosteroid-insensitivity in “innate-type allergy” induced by group 2 innate lymphoid cells (ILC2s).