Immune responses and exacerbations in severe asthma.

Immune responses and exacerbations in severe asthma.
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重症哮喘患者的免疫反应和病情加重。

DOI:
10.1016/j.coi.2021.03.004
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发表时间:
2021-10
影响因子:
7
通讯作者:
Ray A
Ray A
中科院分区:
医学2区
文献类型:
--
作者:
Camiolo MJ;Kale SL;Oriss TB;Gauthier M;Ray A

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哮喘作为一种临床实体,表现出广泛的疾病严重程度。与轻度哮喘不同,吸入皮质类固醇(目前的护理标准)对严重疾病的控制效果不佳。转录组数据以及患者特征和对生物制剂的反应表明,尽管 2 型 (T2) 免疫反应仍然是哮喘的一个不可或缺的特征,但其他分子和免疫因素可能在发病机制中发挥重要作用。 T2 发育机制、T2 细胞因子的细胞来源及其与同时激活的其他免疫途径的关系可能会区分几种不同的亚表型,甚至可能区分哮喘的内型,并对非特异性和靶向抗炎治疗具有不同的反应。最近的数据还表明,源自 T 细胞的非 T2 细胞因子,特别是 IFN-γ 和上皮介质与严重哮喘有关。本综述讨论了这些主题及其与哮喘急性发作的关系。
Asthma as a clinical entity manifests with a broad spectrum of disease severity. Unlike milder asthma, severe disease is poorly controlled by inhaled corticosteroids, the current standard of care. Transcriptomic data, along with patient characteristics and response to biologics show that though Type 2 (T2) immune response remains an integral feature of asthma, additional molecular and immunologic factors may play important roles in pathogenesis. Mechanisms of T2 development, cellular sources of T2 cytokines and their relationship to additional immune pathways concurrently activated may distinguish several different sub-phenotypes, and perhaps endotypes of asthma, with differential response to non-specific and targeted anti-inflammatory therapies. Recent data have also associated non-T2 cytokines derived from T cells, particularly IFN-γ, and epithelial mediators with severe asthma. These topics and their relationships to acute asthma exacerbations are discussed in this review.
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