Unità Operativa Complessa di Pneumologia, Dipartimento di Scienze Biomediche, Odontoiatriche e delle Immagini Morfologiche e Funzionali (BIOMORF), University of Messina, Italy.
Unità Operativa Complessa di Pneumologia, Dipartimento di Scienze Biomediche, Odontoiatriche e delle Immagini Morfologiche e Funzionali (BIOMORF), University of Messina, Italy.
Chest. 2018 Jun;153(6):1424-1431. doi: 10.1016/j.chest.2017.10.033. Epub 2017 Nov 8.
COPD is a leading cause of morbidity and mortality worldwide. Long-term cigarette smoking is the cause of > 90% of COPD cases in Westernized countries. However, only a fraction of chronic heavy smokers develop symptomatic COPD by age 80. COPD is characterized by an abnormal immune response in the lower airways, and its progression is associated with infiltration of the lung by innate and adaptive inflammatory immune cells that form lymphoid follicles. There is growing evidence that both cellular- and antibody-mediated autoimmunity has a fundamental role in the pathogenesis of stable COPD. In particular, carbonyl-modified proteins may help to drive autoimmunity in COPD and cause the characteristic small airways abnormalities and even contribute to the pathogenesis of pulmonary emphysema. Although direct, indirect, and circumstantial evidence of a role for autoimmunity in stable patients with COPD has been identified, no cause-and-effect relationship between autoimmunity and the mechanisms of COPD has been firmly established in man. As such, the potential contribution of an autoimmune response to the pathogenesis of COPD exacerbation is still being investigated and represents an area of active research. Many drugs targeting autoimmune responses are already available, and the results of controlled clinical trials are awaited with great interest. The potential for measuring specific serum autoantibodies as biomarkers to predict clinical phenotypes or progression of stable COPD is promising.
COPD 是全球范围内导致发病率和死亡率的主要原因。长期吸烟是导致西方发达国家 90%以上 COPD 病例的原因。然而，只有少数慢性重度吸烟者在 80 岁之前发展为有症状的 COPD。COPD 的特征是下呼吸道异常的免疫反应，其进展与固有和适应性炎症免疫细胞浸润肺部形成淋巴滤泡有关。越来越多的证据表明，细胞和抗体介导的自身免疫在稳定型 COPD 的发病机制中起着根本性作用。特别是羰基修饰蛋白可能有助于驱动 COPD 中的自身免疫，并导致特征性小气道异常，甚至有助于肺气肿的发病机制。尽管已经确定了自身免疫在稳定型 COPD 患者中的直接、间接和间接证据，但在人类中尚未确定自身免疫与 COPD 机制之间的因果关系。因此，自身免疫反应对 COPD 加重发病机制的潜在贡献仍在研究中，这是一个活跃的研究领域。已经有许多针对自身免疫反应的药物，人们非常感兴趣地等待着对照临床试验的结果。测量特定血清自身抗体作为预测稳定型 COPD 临床表型或进展的生物标志物的潜力是有希望的。
