IMPAIRED INTRACELLULAR-TRANSPORT OF CLASS-I MHC ANTIGENS AS A POSSIBLE MEANS FOR ADENOVIRUSES TO EVADE IMMUNE SURVEILLANCE
IMPAIRED INTRACELLULAR-TRANSPORT OF CLASS-I MHC ANTIGENS AS A POSSIBLE MEANS FOR ADENOVIRUSES TO EVADE IMMUNE SURVEILLANCE
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DOI：
10.1016/0092-8674(85)90026-1
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发表时间：
1985-01-01
期刊：
影响因子：
64.5
通讯作者：
PETERSON, PA
中科院分区：
文献类型：
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作者：
ANDERSSON, M;PAABO, S;PETERSON, PA
腺病毒-2的早期E3区编码一种与I类MHC抗原相关的糖蛋白E19。脉冲追逐和Endo H消化实验表明，这种相互作用伴随着I类抗原重链末端糖基化的消除。此外，病毒蛋白在整个追逐过程中都保留在高甘露糖中。这些结果并不反映膜蛋白末端糖基化的普遍损伤。免疫荧光分析表明，在病毒感染的细胞中，E19和I类抗原在核周区域聚集。I类抗原逐渐从细胞表面消失。I类抗原的细胞表面表达减少可能是腺病毒逃避免疫监视的一种手段。
Early region E3 of adenovirus-2 encodes a glycoprotein, E19, that associates with class I MHC antigens. The interaction occurs concomitantly with abrogated terminal glycosylation of class I antigen heavy chains, as shown by pulse-chase and Endo H digestion experiments. Also the viral protein remains in the high mannose from throughout the chase period. These results do not reflect a general impairment of terminal glycosylation of membrane proteins. Immunofluorescence analyses demonstrated that in virally infected cells E19 and class I antigens accumulate in the perinuclear region. Class I antigens gradually disappear from the cell surface. A diminished cell surface expression of class I antigens may be a means by which adenoviruses evade immune surveillance.