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Immunologic mechanisms in asthma.
Seminars in Immunology ( IF 7.8 ) Pub Date : 2019-11-06 , DOI: 10.1016/j.smim.2019.101333
Tadech Boonpiyathad 1 , Zeynep Celebi Sözener 2 , Pattraporn Satitsuksanoa 3 , Cezmi A Akdis 3
Affiliation  

Asthma is a chronic airway disease, which affects more than 300 million people. The pathogenesis of asthma exhibits marked heterogeneity with many phenotypes defining visible characteristics and endotypes defining molecular mechanisms. With the evolution of novel biological therapies, patients, who do not-respond to conventional asthma therapy require novel biologic medications, such as anti-IgE, anti-IL-5 and anti-IL4/IL13 to control asthma symptoms. It is increasingly important for physicians to understand immunopathology of asthma and to characterize asthma phenotypes. Asthma is associated with immune system activation, airway hyperresponsiveness (AHR), epithelial cell activation, mucus overproduction and airway remodeling. Both innate and adaptive immunity play roles in immunologic mechanisms of asthma. Type 2 asthma with eosinophilia is a common phenotype in asthma. It occurs with and without visible allergy. The type 2 endotype comprises; T helper type 2 (Th2) cells, type 2 innate lymphoid cells (ILC2), IgE-secreting B cells and eosinophils. Eosinophilic nonallergic asthma is ILC2 predominated, which produces IL-5 to recruit eosinophil into the mucosal airway. The second major subgroup of asthma is non-type 2 asthma, which contains heterogeneous group of endoypes and phenotypes, such as exercise-induced asthma, obesity induced asthma, etc. Neutrophilic asthma is not induced by allergens but can be induced by infections, cigarette smoke and pollution. IL-17 which is produced by Th17 cells and type 3 ILCs, can stimulate neutrophilic airway inflammation. Macrophages, dendritic cells and NKT cells are all capable of producing cytokines that are known to contribute in allergic and nonallergic asthma. Bronchial epithelial cell activation and release of cytokines, such as IL-33, IL-25 and TSLP play a major role in asthma. Especially, allergens or environmental exposure to toxic agents, such as pollutants, diesel exhaust, detergents may affect the epithelial barrier leading to asthma development. In this review, we focus on the immunologic mechanism of heterogenous asthma phenotypes.



中文翻译:

哮喘的免疫机制。

哮喘是一种慢性呼吸道疾病,影响超过3亿人。哮喘的发病机制表现出明显的异质性,具有定义可见特征的许多表型和定义分子机制的内型。随着新型生物疗法的发展,对常规哮喘治疗无反应的患者需要新型生物药物,例如抗IgE,抗IL-5和抗IL4 / IL13来控制哮喘症状。对医生而言,了解哮喘的免疫病理学和表征哮喘表型变得越来越重要。哮喘与免疫系统激活,气道高反应性(AHR),上皮细胞激活,粘液过度产生和气道重塑有关。先天免疫和适应性免疫均在哮喘的免疫机制中起作用。2型哮喘伴嗜酸性粒细胞增多是哮喘的常见表型。它在有和没有可见过敏的情况下发生。2型内型包括:T辅助2型(Th2)细胞,2型先天淋巴样细胞(ILC2),分泌IgE的B细胞和嗜酸性粒细胞。嗜酸性粒细胞性非过敏性哮喘以ILC2为主,可产生IL-5以将嗜酸性粒细胞募集到粘膜气道中。哮喘的第二大主要亚型是非2型哮喘,它包含异型内异物和表型,例如运动诱发的哮喘,肥胖症诱发的哮喘等。中性粒细胞性哮喘不是由过敏原引起的,但可以由感染,香烟引起烟雾和污染。Th17细胞和3型ILC产生的IL-17可刺激嗜中性气道炎症。巨噬细胞 树突状细胞和NKT细胞都能够产生已知会导致过敏性和非过敏性哮喘的细胞因子。支气管上皮细胞的活化和细胞因子如IL-33,IL-25和TSLP的释放在哮喘中​​起主要作用。尤其是,过敏原或环境中接触有毒物质(例如污染物,柴油机废气,清洁剂)可能会影响上皮屏障,从而导致哮喘的发展。在这篇综述中,我们着眼于异质性哮喘表型的免疫机制。清洁剂可能会影响导致哮喘发展的上皮屏障。在这篇综述中,我们着眼于异质性哮喘表型的免疫机制。清洁剂可能会影响导致哮喘发展的上皮屏障。在这篇综述中,我们着眼于异质性哮喘表型的免疫机制。

更新日期:2019-11-06
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