自身抗体
医学
慢性阻塞性肺病
免疫学
自身免疫
疾病
肺病
抗体
病理
内科学
作者
Rachel L Byrne,Ian Todd,Patrick J. Tighe,Lucy Fairclough
标识
DOI:10.1016/j.imlet.2019.08.007
摘要
Chronic Obstructive Pulmonary Disease (COPD) is a major cause of death worldwide in which the involvement of autoimmunity has been widely investigated and debated. The role of autoantibodies in COPD has been extensively researched in recent years. The aim of this systematic review is to assess the association between autoantibodies and COPD and analyse whether autoantibody levels correlate with disease severity and/or phenotype. PubMed, Embase, OpenGrey and the reference lists of articles were searched. The strongest evidence for an association between autoantibodies and COPD lies with anti-endothelial/epithelial cell autoantibodies (7 studies, all positive), rheumatoid factor autoantibodies (4 studies, all positive), anti-cytokeratin autoantibodies (3 studies, all positive), anti-nuclear autoantibodies (8 studies, 7 positive) and anti-collagen autoantibodies (10 studies, 6 positive). This review also identifies several other autoantibodies which had both positive and negative associations with COPD, however the evidence for these was not as strong and/or the number of studies is low, and further research is required. In particular, a clear case can be made for the potential importance of autoantibodies to carbonylated proteins. The relationship between autoantibody levels and disease severity requires further research with only 17/43 studies investigating this; however, 12 of the studies did show a positive association, making it a promising area for future research. There was also not enough evidence available on the relationship between autoantibody levels and disease phenotype to draw any conclusions, with only 2 studies investigating it (1 positive and 1 negative). This review has shown very promising evidence for the association of several autoantibodies in COPD and has identified those autoantibodies which require further research.
科研通智能强力驱动
Strongly Powered by AbleSci AI