期刊
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
卷 149, 期 2, 页码 467-479出版社
MOSBY-ELSEVIER
DOI: 10.1016/j.jaci.2021.12.769
关键词
T(H)17 cells; corticosteroid insensitivity; severe asthma; type 2 asthma; non-type 2 asthma; airway neutrophilia; IL-17; IL-6; RhoA; Rho-associated kinase
资金
- National Institutes of Health [R01HL116849, 5R21ES029566]
- Nebraska State LB595 Research Program
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.
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.
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