T<sub>H</sub>17 cells and corticosteroid insensitivity in severe asthma.
Where this comes from
- Record sourced from PubMed, PMID 34953791.
- Also identified by DOI 10.1016/j.jaci.2021.12.769 and PMC identifier 8821175.
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Abstract
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<sub>H</sub>17 cell immune responses. T<sub>H</sub>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<sub>H</sub>17 cells in corticosteroid insensitivity of severe asthma and potential targets to treat this endotype of asthma.
Medical subject headings
- Adrenal Cortex Hormones
- Asthma
- Th17 Cells