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石棉沉着病、矽肺和煤工尘肺的免疫发病机制。

Immunopathogenesis of asbestosis, silicosis, and coal workers' pneumoconiosis.

作者信息

Doll N J, Stankus R P, Barkman H W

出版信息

Clin Chest Med. 1983 Jan;4(1):3-14.

PMID:6340926
Abstract

From these discussions, it is apparent that immunologic aberrations occur in several inorganic dust diseases. Although the role of these immunologic mechanisms in disease pathogenesis remains speculative, recent studies demonstrating the regulation of fibroblast proliferation by macrophage and asbestos or silica interaction support a role for this cell type in the immunopathogenesis of disease. Future cellular and humoral investigations of the bronchoalveolar lavage in workers with pneumoconiosis may clarify the immunologic contributions in the development of fibrosis observed in these diseases.

摘要

从这些讨论中可以明显看出,免疫异常在几种无机粉尘疾病中都会出现。尽管这些免疫机制在疾病发病机制中的作用仍具有推测性,但最近的研究表明巨噬细胞与石棉或二氧化硅相互作用可调节成纤维细胞增殖,这支持了这种细胞类型在疾病免疫发病机制中的作用。未来对尘肺病患者支气管肺泡灌洗进行的细胞和体液研究可能会阐明这些疾病中观察到的纤维化发展过程中的免疫作用。

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