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伪狂犬病病毒感染鼠细胞后,细胞表面Dk和Kk主要组织相容性复合体I类蛋白的差异调节

Differential regulation of Dk and Kk major histocompatibility complex class I proteins on the cell surface after infection of murine cells by pseudorabies virus.

作者信息

Sparks-Thissen R L, Enquist L W

机构信息

Department of Molecular Biology, Princeton University, Princeton, New Jersey 08544, USA.

出版信息

J Virol. 1999 Jul;73(7):5748-56. doi: 10.1128/JVI.73.7.5748-5756.1999.

Abstract

After pseudorabies virus (PRV) infection of murine L929 cells, the cell surface expression of major histocompatibility complex (MHC) class I proteins changes such that the total amount of MHC class I molecules remains relatively constant but the levels of the individual alleles Dk and Kk vary. This is an active process involving at least three PRV gene products that act in an allele-specific manner such that cell surface expression of MHC class I Dk is decreased and that of Kk is increased. Our results indicate that an early gene product mediates the overall reduction in Dk protein and a late gene product which is mutant in the attenuated PRV strain Bartha mediates the increase in Kk protein. We provide additional evidence for a third gene product involved in the regulation of the synthesis of both the Dk and Kk proteins. In addition, we show that the early decrease in the Dk protein is not due to a block in synthesis or processing of the complex through the secretory system.

摘要

在伪狂犬病病毒(PRV)感染小鼠L929细胞后,主要组织相容性复合体(MHC)I类蛋白的细胞表面表达发生变化,使得MHC I类分子的总量保持相对恒定,但各个等位基因Dk和Kk的水平有所不同。这是一个活跃的过程,涉及至少三种PRV基因产物,它们以等位基因特异性方式起作用,使得MHC I类Dk的细胞表面表达减少,而Kk的细胞表面表达增加。我们的结果表明,一种早期基因产物介导了Dk蛋白的总体减少,而减毒PRV株Bartha中的一种晚期基因产物发生突变,介导了Kk蛋白的增加。我们为参与调节Dk和Kk蛋白合成的第三种基因产物提供了额外证据。此外,我们表明Dk蛋白的早期减少并非由于分泌系统中复合物合成或加工的阻断。

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