Le Guennec L, Pestre V, Mouthon L
Service de médecine interne, centre de référence pour les vascularités nécrosantes et la sclérodermie systémique, faculté de médecine Paris-Descartes, université Paris-Descartes, hôpital Cochin, AP-HP de Paris, 27 rue du Faubourg-Saint-Jacques, Paris cedex 14, France.
Rev Mal Respir. 2012 Apr;29(4):557-65. doi: 10.1016/j.rmr.2012.02.001. Epub 2012 Mar 23.
Chronic obstructive pulmonary disease (COPD) is an important cause of morbidity and mortality characterized by irreversible airflow limitation involving a reduced caliber of distal airways (less than 2mm) and alveolar destruction. Exposure to tobacco is a major risk factor for COPD, but all smokers do not develop the disease. In addition, there is continued progression of the disease several years after cessation of the exposure. To explain these phenomena, factors involving innate immunity including the release of neutrophil elastase, macrophage metalloproteases, in combination with pro-apoptotic factors, involved in the worsening of the lesions of emphysema and fibrosis of small airways have been described for many years. More recently, it has been proposed at an advanced stage of the disease that an autoimmune reaction directed mainly at elastin could participate to the pathogenesis of the disease. We here review the immunological processes and currently available data on autoimmunity in COPD.
慢性阻塞性肺疾病(COPD)是发病率和死亡率的重要原因,其特征是不可逆的气流受限,涉及远端气道(小于2mm)管径减小和肺泡破坏。接触烟草是COPD的主要危险因素,但并非所有吸烟者都会患此病。此外,在接触停止后的数年里,疾病仍会持续进展。为了解释这些现象,多年来一直有关于涉及先天免疫的因素的描述,包括中性粒细胞弹性蛋白酶、巨噬细胞金属蛋白酶的释放,以及与促凋亡因子相结合,这些因素参与了肺气肿和小气道纤维化病变的恶化。最近,有人提出在疾病的晚期,主要针对弹性蛋白的自身免疫反应可能参与了疾病的发病机制。我们在此综述COPD中的免疫过程以及目前关于自身免疫的可用数据。