Silica, apoptosis, and autoimmunity.
Silica, apoptosis, and autoimmunity.
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DOI：
10.1080/15476910490911922
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发表时间：
2005-07-01
影响因子：
3.3
通讯作者：
Holian, Andrij
中科院分区：
文献类型：
--
作者：
Brown, Jared M;Pfau, Jean C;Holian, Andrij
关于环境暴露在自身免疫性疾病发展中的作用机制，我们知之甚少。然而，有几种环境因素与引发或加速全身性自身免疫性疾病有关，包括汞、碘、氯乙烯、某些药物和结晶二氧化硅。越来越多的流行病学证据支持这一假设，即职业性二氧化硅接触与多种系统性自身免疫性疾病有关，包括硬皮病(SSC)、类风湿性关节炎(RA)、系统性红斑狼疮(SLE)、肾小球肾炎(GN)和小血管炎(SVV)。然而，很少有机制研究二氧化硅暴露和自身免疫性疾病的发生和发展。本文综述了二氧化硅暴露与系统性自身免疫性疾病相关的人类流行病学数据，但重点介绍了二氧化硅可导致自身免疫的发生和进展的可能机制。
Relatively little is known regarding mechanisms of environmental exposures in the development of autoimmune disease. However, several environmental agents are implicated in triggering or accelerating systemic autoimmune disease, including mercury, iodine, vinyl chloride, certain pharmaceuticals, and crystalline silica. There is increasing epidemiological evidence supporting the hypothesis that occupational silica exposure is associated with a variety of systemic autoimmune diseases, including scleroderma (SSc), rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), glomerulonephritis (GN) and small vessel vasculitis (SVV). However, there have been few mechanistic studies examining silica exposure and autoimmune disease initiation and progression. This review summarizes human epidemiology data linking silica exposure with systemic autoimmune disease, but focuses on possible mechanisms by which silica can lead to the development and progression of autoimmunity.