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Metal-induced diffuse lung disease.

机译:金属诱导的弥漫性肺疾病。

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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 susceptibility markers 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.
机译:与弥漫性实质性肺疾病的发展有关的金属数量继续增加。除了肺纤维化,吸入金属微粒还可以引起广泛的肺部疾病,包括反应性气道疾病和癌症。本文重点介绍吸入铍和钴引起的弥漫性实质疾病。关于铍诱导的疾病的免疫发病机理,比任何其他金属诱导的疾病的了解更多。慢性铍病(CBD)是由工作场所接触铍引起的肉芽肿性肺部疾病,其特征是在支气管肺泡灌洗液中积累了铍特异性CD4(+)T细胞。已经确定了与CBD和硬金属肺疾病相关的遗传易感性标志物。 CBD遗传易感性的机制在于某些人白细胞抗原(HLA)-DP分子结合铍并将其呈递到病原CD4(+)T细胞上的能力。对于硬金属肺疾病是否同样如此还未知。相反,在镍过敏受试者中尚未鉴定出HLA等位基因关联。对金属引起的肺部疾病的研究可以研究环境暴露与遗传易感性之间的关系。这些研究将增进我们对金属诱导的疾病的免疫发病机制以及接触这些金属如何导致不可逆的肺纤维化的理解。

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