TH17 cells and corticosteroid insensitivity in severe asthma

Asthma is classically described as having either a type 2 (T2) eosinophilic phenotype or a non-T2 neutrophilic phenotype. T2 asthma usually responds to classical bronchodilation therapy and corticosteroid treatment. Non-T2 neutrophilic asthma is often more severe. Patients with non-T2 asthma or late-onset T2 asthma show poor response to the currently available anti-inflammatory therapies. These therapeutic failures result in increased morbidity and cost associated with asthma and pose a major health care problem. Recent evidence suggests that some non-T2 asthma is associated with elevated T(H)17 cell immune responses. T(H)17 cells producing Il-17A and IL-17F are involved in the neutrophilic inflammation and airway remodeling processes in severe asthma and have been suggested to contribute to the development of subsets of corticosteroid-insensitive asthma. This review explores the pathologic role of T(H)17 cells in corticosteroid insensitivity of severe asthma and potential targets to treat this endotype of asthma.

Automated summary

Asthma can be classified into T2 and non-T2 types, with non-T2 asthma being more severe and often unresponsive to treatment. Recent studies suggest that non-T2 asthma is associated with T(H)17 cell immune responses, which may contribute to corticosteroid insensitivity in asthma.