Bagenstose L M, Salgame P, Monestier M
Department of Microbiology and Immunology, Temple University School of Medicine, Philadelphia, PA 19140, USA.
Immunol Res. 1999;20(1):67-78. doi: 10.1007/BF02786508.
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.
人类接触某些化合物或治疗药物可能会导致自身免疫综合征的发生。汞（Hg）诱导的自身免疫是少数几种化学物质给药会导致对自身抗原的特异性耐受性丧失的动物模型之一。接受亚毒性剂量的汞或其他重金属后，易感小鼠品系会迅速产生针对核仁抗原的高度特异性抗体。此外，这些动物的免疫系统呈现出普遍激活状态，尤其是Th2亚群明显激活，并且会出现伴有免疫球蛋白沉积的短暂性肾小球肾炎。与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假定机制。
