Ziegler H, Thale R, Lucin P, Muranyi W, Flohr T, Hengel H, Farrell H, Rawlinson W, Koszinowski U H
Max von Pettenkofer Institut, Ludwig-Maximilians-Universitat, Munchen, Federal Republic of Germany.
Immunity. 1997 Jan;6(1):57-66. doi: 10.1016/s1074-7613(00)80242-3.
The principle by which mouse cytomegalovirus blocks antigen presentation in the MHC class I pathway was investigated. The responsible gene m152, encoding a type I transmembrane glycoprotein of 40 kDa, is a member of a gene family located in the right-hand terminal region of the 230 kb virus genome. Expression of m152 in murine and human cells arrested the export of mouse class I complexes from the ER-Golgi intermediate compartment/cis-Golgi compartment and inhibited lysis by cytotoxic T cells. The plasma membrane transport of human MHC class I molecules was not affected. The deletion of the cytoplasmic tail of gp40 did not lift its effect on class I molecule export, indicating that this protein differs in its functions from known immunosubversive viral gene products and represents a novel principle by which a herpesvirus shuts off MHC class I function.
对小鼠巨细胞病毒阻断MHC I类途径中抗原呈递的原理进行了研究。负责的基因m152编码一种40 kDa的I型跨膜糖蛋白，是位于230 kb病毒基因组右手末端区域的一个基因家族的成员。m152在鼠类和人类细胞中的表达阻止了小鼠I类复合物从内质网-高尔基体中间区室/顺式高尔基体区室的输出，并抑制了细胞毒性T细胞的裂解作用。人MHC I类分子的质膜转运不受影响。gp40胞质尾的缺失并未消除其对I类分子输出的影响，这表明该蛋白在功能上与已知的免疫颠覆病毒基因产物不同，代表了疱疹病毒关闭MHC I类功能的一种新机制。
