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重金属诱导自身免疫的机制。

Mechanisms of heavy metal-induced autoimmunity.

作者信息

Rowley Benjamin, Monestier Marc

机构信息

Department of Microbiology and Immunology, Temple University School of Medicine, Philadelphia, PA 19140, USA.

出版信息

Mol Immunol. 2005 May;42(7):833-8. doi: 10.1016/j.molimm.2004.07.050.

DOI:10.1016/j.molimm.2004.07.050
PMID:15829271
Abstract

Chemical exposure can trigger or accelerate the development of autoimmune manifestations. Although heavy metals are elementary chemical structures, they can have profound and complex effects on the immune system. In genetically susceptible mice or rats, administration of subtoxic doses of mercury induces both the production of highly specific autoantibodies and a polyclonal activation of the immune system. We review in this article some of the mechanisms by which heavy metal exposure can lead to autoimmunity.

摘要

化学物质暴露可引发或加速自身免疫表现的发展。尽管重金属是基本的化学结构,但它们可对免疫系统产生深远而复杂的影响。在基因易感的小鼠或大鼠中,给予亚毒性剂量的汞可诱导产生高度特异性自身抗体以及免疫系统的多克隆激活。我们在本文中综述了重金属暴露可导致自身免疫的一些机制。

相似文献

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Mechanisms of heavy metal-induced autoimmunity.重金属诱导自身免疫的机制。
Mol Immunol. 2005 May;42(7):833-8. doi: 10.1016/j.molimm.2004.07.050.
2
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Alterations of TH1/TH2 reactivity by heavy metals: possible consequences include induction of autoimmune diseases.重金属对TH1/TH2反应性的改变:可能的后果包括自身免疫性疾病的诱发。
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Nephrotic Syndrome Associated With Heavy Metals Exposure: A Case Report and Literature Review.重金属暴露相关的肾病综合征:一例报告及文献综述
Cureus. 2024 Jan 10;16(1):e52029. doi: 10.7759/cureus.52029. eCollection 2024 Jan.
2
Naturally occurring autoimmune disease in (NZB X NZW) F1 mice is correlated with suppression of MZ B cell development due to aberrant B Cell Receptor (BCR) signaling, which is exacerbated by exposure to inorganic mercury.(新西兰黑鼠×新西兰白鼠)F1代小鼠的自然发生的自身免疫性疾病与由于异常B细胞受体(BCR)信号传导导致的边缘区B细胞发育受抑制相关,而暴露于无机汞会加剧这种情况。
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3
Metabolomics: a promising tool for deciphering metabolic impairment in heavy metal toxicities.
代谢组学:一种用于解读重金属毒性中代谢损伤的有前景的工具。
Front Mol Biosci. 2023 Jul 6;10:1218497. doi: 10.3389/fmolb.2023.1218497. eCollection 2023.
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SN Appl Sci. 2022;4(8):236. doi: 10.1007/s42452-022-05113-w. Epub 2022 Jul 27.
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