Division of Allergy, Asthma, and Immunology, Scripps Clinic, San Diego, CA, United States.
Division of Allergy, Asthma, and Immunology, Scripps Clinic, San Diego, CA, United States.
Curr Opin Immunol. 2020 Oct;66:9-13. doi: 10.1016/j.coi.2020.02.006. Epub 2020 Apr 13.
Aspirin-exacerbated respiratory disease (AERD) classically presents with severe asthma, nasal polyposis, and respiratory exacerbations in response to cyclooxygenase (COX)-1 inhibition. Recent advances in our understanding of AERD have revealed multiple facets of immune dysregulation, including diminished prostaglandin E2 (PGE) function and elevated levels of both cysteinyl leukotrienes (CysLTs) and innate cytokines such as interleukin 33 (IL-33). Inflammatory mediators in AERD heighten the recruitment and activation of innate lymphoid cells type 2 (ILC2), mast cells, eosinophils, and platelet-adherent leukocytes. This contributes to a cyclical pattern of type 2 inflammation. Here, we highlight current understanding of the immunopathogenesis of AERD.
阿司匹林加重的呼吸道疾病（AERD）的特征是严重哮喘、鼻息肉和对环氧化酶（COX）-1 抑制的呼吸道恶化。我们对 AERD 的理解的最新进展揭示了免疫失调的多个方面，包括前列腺素 E2（PGE）功能下降和半胱氨酰白三烯（CysLT）以及先天细胞因子（如白细胞介素 33（IL-33））水平升高。AERD 中的炎症介质会增加 2 型固有淋巴细胞（ILC2）、肥大细胞、嗜酸性粒细胞和血小板黏附白细胞的募集和激活。这导致 2 型炎症的周期性模式。在这里，我们重点介绍对 AERD 的免疫发病机制的当前理解。
