慢性阻塞性肺病
医学
自身免疫
免疫学
发病机制
恶化
自身抗体
免疫系统
抗体
内科学
作者
Gaetano Caramori,Paolo Ruggeri,Antonino Di Stefano,Sharon Mumby,Giuseppe Girbino,Ian M. Adcock,Paul Kirkham
出处
期刊:Chest
[Elsevier]
日期:2018-06-01
卷期号:153 (6): 1424-1431
被引量:54
标识
DOI:10.1016/j.chest.2017.10.033
摘要
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.
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