重症哮喘的免疫反应与急性发作

2021/04/23

   摘要
   哮喘作为一种临床实体,其疾病严重性表现具有较大的不同。与轻症哮喘不同,重症哮喘很难通过吸入糖皮质激素(目前的标准治疗)得到控制。转录组学数据以及患者特征和对生物制剂的反应共同表明,尽管2型(T2)免疫反应仍然是哮喘的一个重要特征,但如分子和免疫因素等其他机制可能在哮喘的发病机制中也发挥重要作用。T2的形成机制、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区分为几种不同的亚型,或者是哮喘的内型,它们对非特异性和靶向抗炎治疗有不同的反应性。最近的数据也表明,T细胞来源的非T2细胞因子,特别是IFN-γ,与重症哮喘的上皮介质有关。这些主题及其与哮喘急性发作的关系将在这篇综述中进行讨论。

 
(中日友好医院呼吸与危重症医学科 顾宪民 摘译 林江涛 审校)
(Curr Opin Immunol.2021 Mar 24;72:34-42.doi: 10.1016/j.coi.2021.03.004.)

 
Immune responses and exacerbations in severe asthma

Matthew J Camiolo, Sagar L Kale, Timothy B Oriss, Marc Gauthier, Anuradha Ray.

Abstract
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 subphenotypes, 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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