Ni Ling, Dong Chen
Institute for Immunology and School of Medicine, Tsinghua University, Beijing, China.
Front Immunol. 2018 Jun 21;9:1431. doi: 10.3389/fimmu.2018.01431. eCollection 2018.
Chronic obstructive pulmonary disease (COPD) is currently the third largest cause of human mortality in the world after stroke and heart disease. COPD is characterized by sustained inflammation of the airways, leading to destruction of lung tissue and declining pulmonary function. The main risk factor is known to be cigarette smoke currently. However, the strategies for prevention and treatment have not altered significantly for many years. A growing body of evidences indicates that the immune system plays a pivotal role in the pathogenesis of COPD. The repeated and progressive activation of immune cells is at least in part the source of this chronic inflammation. In this review paper, we have conducted an extensive literature search of the studies of immune cells in COPD patients. The objective is to assess the contributions of different immune cell types, the imbalance of pro/anti-inflammatory immune cells, such as M1/M2 macrophages, Tc1/Tc10, and Th17/Treg, and their mediators in the peripheral blood as well as in the lung to the pathogenesis of COPD. Therefore, understanding their roles in COPD development will help us find the potential target to modify this disease. This review focuses predominantly on data derived from human studies but will refer to animal studies where they help understand the disease in humans.
慢性阻塞性肺疾病（COPD）目前是全球继中风和心脏病之后的第三大致死原因。COPD的特征是气道持续炎症，导致肺组织破坏和肺功能下降。目前已知主要危险因素是香烟烟雾。然而，多年来预防和治疗策略并未发生显著改变。越来越多的证据表明，免疫系统在COPD的发病机制中起关键作用。免疫细胞的反复和渐进性激活至少部分是这种慢性炎症的来源。在这篇综述文章中，我们对COPD患者免疫细胞的研究进行了广泛的文献检索。目的是评估不同免疫细胞类型、促炎/抗炎免疫细胞失衡，如M1/M2巨噬细胞、Tc1/Tc10以及Th17/Treg及其介质在COPD患者外周血和肺中对发病机制的贡献。因此，了解它们在COPD发展中的作用将有助于我们找到改变这种疾病的潜在靶点。本综述主要关注来自人体研究的数据，但在有助于理解人类疾病的情况下也会参考动物研究。
