Chronic Obstructive Pulmonary Disease 1 New insights into the immunology of chronic obstructive pulmonary disease
Chronic Obstructive Pulmonary Disease 1 New insights into the immunology of chronic obstructive pulmonary disease
复制标题
DOI：
10.1016/s0140-6736(11)60988-4
复制
发表时间：
2011-09-10
期刊：
影响因子：
168.9
通讯作者：
Bracke, Ken R.
中科院分区：
文献类型：
--
作者：
Brusselle, Guy G.;Joos, Guy F.;Bracke, Ken R.
慢性阻塞性肺疾病（COPD）是一种与肺部对有害颗粒和气体的异常炎症免疫反应相关的异质性综合征。香烟烟雾通过触发模式识别受体，直接或间接地通过应激或死亡细胞释放与损伤相关的分子模式，激活固有免疫细胞，如上皮细胞和巨噬细胞。活化的树突状细胞诱导适应性免疫反应，包括辅助性T细胞（Th1和Th17） CD4+ T细胞、CD8+细胞毒性和b细胞反应，从而导致慢性炎症的淋巴滤泡发育。病毒和细菌感染不仅会导致慢性阻塞性肺病急性加重，还会通过病原体相关的分子模式放大和延续稳定期慢性阻塞性肺病的慢性炎症。我们讨论了自身免疫（自身抗体）、重塑、细胞外基质来源碎片、先天肺防御受损、氧化应激、缺氧和microrna失调在戒烟后肺部炎症持续中的作用。
Chronic obstructive pulmonary disease (COPD) is a heterogeneous syndrome associated with abnormal inflammatory immune responses of the lung to noxious particles and gases. Cigarette smoke activates innate immune cells such as epithelial cells and macrophages by triggering pattern recognition receptors, either directly or indirectly via the release of damage-associated molecular patterns from stressed or dying cells. Activated dendritic cells induce adaptive immune responses encompassing T helper (Th1 and Th17) CD4+ T cells, CD8+ cytotoxicity, and B-cell responses, which lead to the development of lymphoid follicles on chronic inflammation. Viral and bacterial infections not only cause acute exacerbations of COPD, but also amplify and perpetuate chronic inflammation in stable COPD via pathogen-associated molecular patterns. We discuss the role of autoimmunity (autoantibodies), remodelling, extracellular matrix-derived fragments, impaired innate lung defences, oxidative stress, hypoxia, and dysregulation of microRNAs in the persistence of the pulmonary inflammation despite smoking cessation.