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氯化汞诱导的棕色挪威大鼠免疫复合物型疾病:易感性的遗传控制

Immune complex type disease induced by HgCl2 in Brown-Norway rats: genetic control of susceptibility.

作者信息

Sapin C, Mandet C, Druet E, Gunther E, Druet P

出版信息

Clin Exp Immunol. 1982 Jun;48(3):700-4.

Abstract

Mercuric chloride induces a biphasic autoimmune glomerulonephritis in Brown-Norway (BN) rats but not in Lewis (LEW) rats. The genetic control of susceptibility to both phases was investigated by testing the response of segregants between BN and LEW rats and of congenic LEW.1N rats. It was confirmed that susceptibility to the first phase, characterized by the appearance of anti-glomerular basement membrane antibodies, depends on several genes one of which is RT1 linked. Susceptibility to the second phase, which is an immune complex type glomerulonephritis, was found to depend on one major RT1 linked gene or cluster of genes with a role for other(s) non-RT1 linked gene(s) controlling the magnitude of the response. However, congenic LEW.1N rats were found to be resistant. This suggests that the disease gene has been lost during the strain derivation. The question of whether both phases are two different diseases or expression of the same process cannot be definitely answered; data however indicate a dissociation of both disease processes.

摘要

氯化汞可在棕色挪威(BN)大鼠中诱发双相自身免疫性肾小球肾炎,但在刘易斯(LEW)大鼠中则不会。通过检测BN大鼠和LEW大鼠之间的分离后代以及同源LEW.1N大鼠的反应,研究了对两个阶段易感性的遗传控制。已证实,以抗肾小球基底膜抗体出现为特征的第一阶段易感性取决于多个基因,其中一个与RT1相关。发现对第二阶段(即免疫复合物型肾小球肾炎)的易感性取决于一个主要的与RT1相关的基因或基因簇,以及其他一些控制反应程度的非RT1相关基因。然而,发现同源LEW.1N大鼠具有抗性。这表明该疾病基因在品系衍生过程中丢失了。两个阶段是两种不同疾病还是同一过程的表现这一问题无法得到明确解答;然而,数据表明这两个疾病过程是分离的。

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本文引用的文献

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