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非 2 型哮喘的发病机制。

Mechanisms of non-type 2 asthma.

机构信息

Division of Allergy and Immunology, Department of Internal Medicine, University of South Florida, Morsani College of Medicine and the James A. Haley Veterans' Hospital, Tampa, FL, USA.

Division of Allergy and Immunology, Department of Internal Medicine, University of South Florida, Morsani College of Medicine and the James A. Haley Veterans' Hospital, Tampa, FL, USA.

出版信息

Curr Opin Immunol. 2020 Oct;66:123-128. doi: 10.1016/j.coi.2020.10.002. Epub 2020 Nov 4.

DOI:10.1016/j.coi.2020.10.002
PMID:33160187
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7852882/
Abstract

Non-type 2 inflammation (Non-T2)-mediated asthma is difficult to define due to lack of signature biomarkers. It exists in the absence of T2-high or eosinophilic inflammation and includes neutrophilic and paucigranulocytic subtypes. Several cell types and cytokines, including Th1, Th17, IL-6, and IL-17, contribute to mechanisms of non-T2 asthma. Neutrophil extracellular traps (NETs) and inflammasome activation likely play a role in severe neutrophilic asthma. Several mechanisms lead to uncoupling of airway hyperresponsiveness and remodeling from airway inflammation in paucigranulocytic asthma. Recent research on transcriptomics and proteomics in non-T2 asthma is discussed in this review. Investigations of specific drug therapies for non-T2 asthma have been disappointing, and remain an important area for future clinical studies.

摘要

由于缺乏特征性生物标志物,非 2 型炎症(非 T2)介导的哮喘难以定义。它存在于 T2 高或嗜酸性粒细胞炎症缺失的情况下,包括中性粒细胞和寡粒细胞亚型。几种细胞类型和细胞因子,包括 Th1、Th17、IL-6 和 IL-17,有助于非 T2 哮喘的发生机制。中性粒细胞细胞外陷阱(NETs)和炎症小体激活可能在严重中性粒细胞性哮喘中发挥作用。几种机制导致在寡粒细胞性哮喘中,气道高反应性和重塑与气道炎症脱耦联。本文综述了非 T2 哮喘中转录组学和蛋白质组学的最新研究。针对非 T2 哮喘的特定药物治疗的研究令人失望,仍然是未来临床研究的一个重要领域。

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