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在CD4缺陷小鼠中病毒特异性主要组织相容性复合体II类限制性CD8 + 细胞毒性T细胞的激活。

Activation of virus-specific major histocompatibility complex class II-restricted CD8+ cytotoxic T cells in CD4-deficient mice.

作者信息

Heemskerk M H, Schilham M W, Schoemaker H M, Spierenburg G, Spaan W J, Boog C J

机构信息

Institute of Infectious Diseases and Immunology, Faculty of Veterinary Medicine, University of Utrecht, The Netherlands.

出版信息

Eur J Immunol. 1995 Apr;25(4):1109-12. doi: 10.1002/eji.1830250438.

DOI:10.1002/eji.1830250438
PMID:7737281
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7163489/
Abstract

Acute enteritic or respiratory disease is a consequence of coronavirus infection in man and rodents. Mouse hepatitis virus, stain A59 (MHV-A59) causes acute hepatitis in mice and rats and induces a response of major histocompatibility complex (MHC) class II-restricted CD4+ cytotoxic T cells, protecting mice against acute infection. In the present study we show that MHV-A59 infection of mice that lack a functional CD4 gene activates effector cells of the CD8+ phenotype. These cytotoxic T cells lyse virus-infected target cells in a MHC class II-restricted fashion. The results indicate that CD8+ T cells have the potential to utilize MHC class II as restriction element, illustrating that the immune system can effectively deal with evading microorganisms, such as viruses which down-regulate MHC class I.

摘要

急性肠道或呼吸道疾病是人类和啮齿动物感染冠状病毒的结果。小鼠肝炎病毒A59株(MHV-A59)可引起小鼠和大鼠的急性肝炎,并诱导主要组织相容性复合体(MHC)II类限制性CD4+细胞毒性T细胞反应,保护小鼠免受急性感染。在本研究中,我们发现感染缺乏功能性CD4基因的小鼠的MHV-A59激活了CD8+表型的效应细胞。这些细胞毒性T细胞以MHC II类限制性方式裂解病毒感染的靶细胞。结果表明,CD8+T细胞有潜力利用MHC II类作为限制元件,说明免疫系统能够有效应对逃避微生物,如下调MHC I类的病毒。

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本文引用的文献

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