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학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
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연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2024.4
- 수록면
- 194 - 201 (8page)
- DOI
- 10.3349/ymj.2023.0432
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초록· 키워드
오류제보하기
Severe asthma (SA) has heterogeneous inflammatory phenotypes characterized by persistent airway inflammation (eosinophilic and/or neutrophilic inflammation) and remodeling. Various immune cells (eosinophils, neutrophils, and macrophages) become more activated and release inflammatory mediators and extracellular traps, damaging the protective barrier of airway epithelial cells and further activating other immune and structural cells. These cells play a role in autoimmune responses in asthmatic air ways, where the adaptive immune system generates autoantibodies, inducing immunoglobulin G-dependent airway inflamma tion. Recent studies have suggested that adult asthmatics had high titers of autoantibodies associated with asthma severity, al though pathogenic factors or diagnostic criteria are not well-defined. This challenge is further compounded by asthmatics with the autoimmune responses showing therapy insensitivity or failure to current pharmacological and biological treatment. This re view updates emerging mechanisms of autoimmune responses in asthmatic airways and provides insights into their roles, pro posing potential biomarkers and therapeutic targets for SA.
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