The autoimmune response induced by mouse hepatitis virus A59 is expanded by a hepatotoxic agent.
The autoimmune response induced by mouse hepatitis virus A59 is expanded by a hepatotoxic agent.
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DOI：
10.1016/j.intimp.2009.02.006
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发表时间：
2009-05
影响因子：
5.6
通讯作者：
Retegui LA
中科院分区：
文献类型：
--
作者：
Aparicio JL;Duhalde-Vega M;Loureiro ME;Retegui LA
小鼠肝炎病毒株A59（MHV-A59）在几种小鼠品系中引发各种病理，包括高丙种球蛋白血症、肝炎和胸腺退化。我们以前报告的存在下，肝和肾延胡索酰乙酰乙酸水解酶（FAH）的自身抗体（autoAb）从MHV-A59感染的小鼠血清中。长期MHV感染的小鼠代表了非致病性自身免疫应答的良好模型，因为尽管存在自身抗体，但动物显然是健康的。这项工作的目的是观察释放内源性佐剂（即危险信号）的严重肝损伤是否会引起更广泛的自身抗体，并可能引起自身免疫性肝炎的迹象。小鼠感染MHV后30天，腹腔注射四氯化碳（CCl_4），20天后检测血清自身抗体和总IgG。MHV感染与CCl 4毒性作用的相关性导致高丙种球蛋白血症和针对各种肝脏和肾脏蛋白的自身抗体的产生。肝组织学检查显示组织损伤，但提交给MHV + CCl 4的动物与对照组之间没有显著差异，对照组要么被MHV感染而没有CCl 4，要么在没有MHV感染的情况下被CCl 4中毒。这些结果表明，病毒感染后的肝损伤可能导致免疫应答的扩散和血清IgG的增加，表明本文所用的方法可以模拟自身免疫性肝炎的发作。
Mouse hepatitis virus strain A59 (MHV-A59) triggers various pathologies in several mouse strains, including hypergammaglobulinaemia, hepatitis and thymus involution. We reported previously the presence of autoantibodies (autoAb) to liver and kidney fumarylacetoacetate hydrolase (FAH) in sera from mice infected with MHV-A59. Long-term MHV-infected mice represented a good model of non-pathogenic autoimmune response since the animals were apparently healthy in spite of the presence of autoAb. The aim of this work was to see whether a severe liver injury, which releases endogenous adjuvants, i.e. danger signals, could elicit a broader spectrum of autoAb and perhaps signs of autoimmune hepatitis. Carbon tetrachloride (CCl4) was injected into mice 30 days after MHV infection, and serum was assayed for autoAb and total IgG 20 days later. The association of MHV infection with the toxic effects of CCl4 resulted in hypergammaglobulinaemia and the production of autoAb to various liver and kidney proteins. Histological examination of liver samples showed tissue damages but without significant differences between the animals submitted to MHV + CCl4 and controls, which were either infected by MHV without CCl4, or poisoned by CCl4 in the absence of MHV infection. Those results show that liver injury after viral infection may lead to the spreading of the immune response and to an increase of serum IgG, suggesting that the procedure used herein could simulate the onset of autoimmune hepatitis.
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