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Effect of a retroviral immunodeficiency syndrome on murine cytomegalovirus-induced hepatitis

机译:逆转录病毒免疫缺陷综合征对小鼠巨细胞病毒性肝炎的影响

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摘要

We have studied the effects of LP-BM5 MuLV-induced murine acquired immunodeficiency syndrome (MAIDS) on concomitant murine cytomegalovirus (MCMV) infection in the livers of C57BL mice. A delayed inflammatory response in livers of mice with MAIDS (M+) on day 4 was associated with impaired clearance of MCMV-infected cells 6 days after infection. This correlated with increased levels of inflammation and serum alanine transaminase. The latter reflects enhanced hepatic necrosis, which was evident histologically. Delayed-type hypersensitivity responses to MCMV antigen were unimpaired in M+ mice and were mediated by CD8+ cells. Depletion of NK1.1+ cells from M+ mice increased MCMV replication and associated liver damage on day 6, whereas CD8+ depletion had little effect. In contrast, in the presence of CD8+ cells M- C57BL mice did not require NK1.1+ cells for control of hepatic MCMV infection, but dual NK1.1+ and CD8+ depletion dramatically potentiated hepatic MCMV replication. Our results suggest that M+ mice may acquire non-NK1.1+ and non-CD8+ cells that are able to partially control hepatic MCMV infection. These findings are discussed with reference to mortality in M+ mice after high-dose MCMV infection, as this is initially delayed but ultimately higher than in M- controls.
机译:我们已经研究了LP-BM5 MuLV诱导的小鼠获得性免疫缺陷综合症(MAIDS)对C57BL小鼠肝脏中伴随的小鼠巨细胞病毒(MCMV)感染的影响。在感染后6天,患有MAIDS(M +)的小鼠肝脏中的炎症反应延迟,与MCMV感染细胞的清除受损有关。这与炎症和血清丙氨酸转氨酶水平升高有关。后者反映出增强的肝坏死,这在组织学上是明显的。在M +小鼠中对MCMV抗原的迟发型超敏反应不受损害,并由CD8 +细胞介导。在第6天,耗尽M +小鼠的NK1.1 +细胞会增加MCMV复制和相关的肝损害,而耗尽CD8 +的影响很小。相比之下,在存在CD8 +细胞的情况下,M-C57BL小鼠不需要NK1.1 +细胞来控制肝MCMV感染,但是NK1.1 +和CD8 +的双重消耗会显着增强肝MCMV复制。我们的结果表明,M +小鼠可能获得能够部分控制肝MCMV感染的非NK1.1 +和非CD8 +细胞。参考高剂量MCMV感染后M +小鼠的死亡率讨论了这些发现,因为这最初被延迟了,但最终高于M-对照。

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  • 来源
    《The American Journal of Pathology》 |1997年第3期|p.1089-1100|共12页
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    Craig Douglas Peacock, Stuart Desmond Olver, and Patricia Price From the Department of Microbiology, University of Western Australia, Nedlands, Australia Supported by the National Health and Medical Research Council of Australia (NH&MRC 0415054211) and a Commonwealth AIDS research grant. Accepted for publication November 18, 1996. Address reprint requests to Mr. Craig Peacock, Department of Microbiology, University of Western Australia, Nedlands, WA 6009, Australia.;

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