Metal-Induced Diffuse Lung Disease

被引:14
作者
Fontenot, Andrew P. [1 ,2 ]
Amicosante, Massimo [3 ]
机构
[1] Univ Colorado, Hlth Sci Ctr, Dept Med, Denver, CO 80262 USA
[2] Univ Colorado, Hlth Sci Ctr, Dept Immunol, Denver, CO 80262 USA
[3] Univ Roma Tor Vergata, Dept Internal Med, Rome, Italy
关键词
Lung; metals; T cells; genetic susceptibility; fibrosis; granuloma;
D O I
10.1055/s-0028-1101276
中图分类号
R4 [临床医学];
学科分类号
1002 ; 100602 ;
摘要
The number of metals that are associated with the development of diffuse parenchymal lung disease continues to expand. In addition to lung fibrosis, inhalation of metal particulates can induce a wide range of lung pathology, including reactive airways disease and cancer. This article focuses on diffuse parenchymal diseases resulting from the inhalation of beryllium and cobalt. More is known regarding the immunopathogenesis of beryllium-induced disease than is known for disease induced by any other metal. Chronic beryllium disease (CBD) is a granulomatous lung disorder caused by beryllium exposure in the workplace and is characterized by the accumulation of beryllium-specific CD4(+) T cells in the bronchoalveolar lavage. Genetic susceptibibty markets associated with increased risk have been identified for both CBD and hard metal lung disease. The mechanism for the genetic susceptibility of CBD lies in the ability of certain human leukocyte antigen (HLA)-DP molecules to bind and present beryllium to pathogenic CD4(+) T cells. Whether the same is true for hard metal lung disease is unknown. In contrast, no HLA allelic association has been identified in nickel allergic Subjects. The study of metal-induced lung disease allows the investigation of the relationship between environmental exposure and genetic susceptibility. These studies will enhance our understanding of the immunopathogenesis of metal-Induced disease and how exposure to these metals results in irreversible lung fibrosis.
引用
收藏
页码:662 / 669
页数:8
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