Laboratory of Immunoregulation, VIB-UGent Center for Inflammation Research, Ghent, Belgium.
Department of Internal Medicine, Ghent University, Ghent, Belgium.
Front Immunol. 2018 Sep 4;9:2006. doi: 10.3389/fimmu.2018.02006. eCollection 2018.
Asthma is a common lung disease affecting 300 million people worldwide. Allergic asthma is recognized as a prototypical Th2 disorder, orchestrated by an aberrant adaptive CD4+ T helper (Th2/Th17) cell immune response against airborne allergens, that leads to eosinophilic inflammation, reversible bronchoconstriction, and mucus overproduction. Other forms of asthma are controlled by an eosinophil-rich innate ILC2 response driven by epithelial damage, whereas in some patients with more neutrophilia, the disease is driven by Th17 cells. Dendritic cells (DCs) and macrophages are crucial regulators of type 2 immunity in asthma. Numerous lipid mediators including the eicosanoids prostaglandins and leukotrienes influence key functions of these cells, leading to either pro- or anti-inflammatory effects on disease outcome. In this review, we will discuss how eicosanoids affect the functions of DCs and macrophages in the asthmatic lung and how this leads to aberrant T cell differentiation that causes disease.
哮喘是一种常见的肺部疾病，影响着全球 3 亿人。过敏性哮喘被认为是一种典型的 Th2 失调疾病，由针对空气传播过敏原的异常适应性 CD4+ T 辅助（Th2/Th17）细胞免疫反应引发，导致嗜酸性粒细胞炎症、可逆性支气管收缩和黏液过度产生。其他形式的哮喘由上皮损伤驱动的富含嗜酸性粒细胞的先天 ILC2 反应控制，而在一些中性粒细胞较多的患者中，疾病由 Th17 细胞驱动。树突状细胞（DCs）和巨噬细胞是哮喘中 2 型免疫的关键调节剂。许多脂质介质，包括前列腺素和白三烯等类二十烷酸，影响这些细胞的关键功能，导致对疾病结局产生促炎或抗炎作用。在这篇综述中，我们将讨论类二十烷酸如何影响哮喘肺部中 DCs 和巨噬细胞的功能，以及这如何导致导致疾病的异常 T 细胞分化。
