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严重哮喘中的 T17 细胞和皮质类固醇不敏感性。

T17 cells and corticosteroid insensitivity in severe asthma.

机构信息

Department of Pharmacology and Neuroscience, Creighton University School of Medicine, Omaha, Neb.

Department of Internal Medicine, University of South Florida School of Medicine, Tampa, Fla.

出版信息

J Allergy Clin Immunol. 2022 Feb;149(2):467-479. doi: 10.1016/j.jaci.2021.12.769. Epub 2021 Dec 23.

DOI:10.1016/j.jaci.2021.12.769
PMID:34953791
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8821175/
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 T17 cell immune responses. T17 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 T17 cells in corticosteroid insensitivity of severe asthma and potential targets to treat this endotype of asthma.

摘要

哮喘通常被描述为具有 2 型(T2)嗜酸性表型或非 T2 中性粒细胞表型。T2 哮喘通常对经典的支气管扩张治疗和皮质类固醇治疗有反应。非 T2 中性粒细胞性哮喘通常更严重。非 T2 哮喘或迟发性 T2 哮喘患者对目前可用的抗炎治疗反应不佳。这些治疗失败导致哮喘相关发病率和成本增加,并构成重大的医疗保健问题。最近的证据表明,一些非 T2 哮喘与升高的 T17 细胞免疫反应有关。产生 IL-17A 和 IL-17F 的 T17 细胞参与严重哮喘的中性粒细胞炎症和气道重塑过程,并被认为有助于皮质类固醇不敏感哮喘亚群的发展。这篇综述探讨了 T17 细胞在严重哮喘皮质类固醇不敏感中的病理作用以及治疗这种哮喘表型的潜在靶点。

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