免疫系统中氧化还原细胞信号的金属诱导调节

W. Lutz, W. Wąsowicz
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引用次数: 5

摘要

环境中的大量金属进入人体,对免疫系统形成细胞产生多种毒性作用。这些作用可能通过负责细胞凋亡或坏死的机制以及激活或抑制免疫功能导致细胞死亡。淋巴细胞和抗原呈递细胞的激活或抑制取决于靶细胞中金属的种类和浓度。在免疫毒性作用中,主要是由金属引起的蛋白质活性的变化诱导信号通路,以及能够调节细胞因子及其受体和表面粘附分子等蛋白质分子产生的基因的表达变化。这些蛋白质的激活不足或产生受到抑制表现为机体免疫力下降(免疫抑制),而它们的过度激活则引起超敏反应(过敏、自身免疫)。越来越多的数据证实,参与细胞信号传导的蛋白的激活和参与免疫应答的蛋白合成调控基因表达的激活与免疫细胞的氧化代谢有关。这些数据也提供了证据,表明金属对免疫反应的调节作用是通过影响控制活性氧产生的机制来进行的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Metal-Induced Modulation of Redox Cell-Signaling in the Immune System
A large number of metals in the environment enter the human body and exert diverse toxic effects on the immune system-forming cells. These effects may lead to the death of the cells through the mechanism responsible for apoptosis or necrosis, as well as for activation or suppression of immune functions. Activation or suppression of lymphocytes and antigen-presenting cells depends on the kind and concentration of metals in target cells. The metal-generated changes in protein activity, which induce signaling pathways, as well as changes in expression of genes able to regulate the production of such protein molecules as cytokines and their receptors and surface adhesion molecules, predominate in the immunotoxic effects. Insufficient activation or inhibited production of these proteins is manifested by a decreased immunity of the organism (immuno-suppression), whereas their overactivation induces hypersensitivity (allergy, autoimmunization). A growing amount of data confirm that the activation of proteins involved in cellular signaling and the activation of expression of genes regulating the synthesis of proteins participating in the immune response are associated with oxidative metabolism of immune cells. These data also provide evidence that the modulation effect of metals on the immune response proceeds through influencing the mechanisms that control the production of reactive oxygen species.
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