Murine mercury-induced autoimmunity -: A model of chemically related autoimmunity in humans
Murine mercury-induced autoimmunity -: A model of chemically related autoimmunity in humans
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DOI：
10.1007/bf02786508
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发表时间：
1999-01-01
影响因子：
4.4
通讯作者：
Monestier, M
中科院分区：
文献类型：
--
作者：
Bagenstose, LM;Salgame, P;Monestier, M
人体暴露于某些化合物或治疗药物可导致自身免疫综合征的发展。汞（Hg）诱导的自身免疫是为数不多的动物模型之一，在这种动物模型中，化学物质的施用会导致特定的丧失；对自身抗原的耐受性。在接受亚毒性剂量的汞或其他重金属后，易感小鼠品系迅速产生针对核仁抗原的高度特异性抗体。此外，这些动物表现出免疫系统的普遍激活，特别是Th2亚群和伴有免疫球蛋白沉积的短暂性肾小球肾炎。像许多人类自身免疫性疾病一样，这种综合征与易感主要组织相容性复合体（MHC） II类基因的表达有关。在本文中，我们回顾了该模型的基本特征，并讨论了汞造成如此严重免疫功能障碍的可能机制。
Human exposure to certain compounds or therapeutic drugs can result in the development of an autoimmune syndrome. Mercury (Hg) induced autoimmunity is one of the few animal models in which administration of a chemical induces a specific loss of; tolerance to self-antigens. After receiving subtoxic doses of Hg or other heavy metals, susceptible mouse strains rapidly develop highly specific antibodies to nucleolar antigens. In addition, these animals display a general activation of the immune system, especially pronounced for the Th2 subset and a transient glomerulonephritis with immunoglobulin deposits. Like many human autoimmune diseases, this syndrome is associated with the expression of susceptible major histocompatibility complex (MHC) class II genes. In this article, we review the essential features of this model, and we discuss the putative mechanisms by which Hg creates such a severe immune dysfunction.