A mouse cytomegalovirus glycoprotein, gp34, forms a complex with folded class I MHC molecules in the ER which is not retained but is transported to the cell surface
A mouse cytomegalovirus glycoprotein, gp34, forms a complex with folded class I MHC molecules in the ER which is not retained but is transported to the cell surface
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DOI：
10.1093/emboj/16.4.685
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发表时间：
1997-02-17
期刊：
影响因子：
11.4
通讯作者：
Ploegh, HL
中科院分区：
文献类型：
--
作者：
Kleijnen, MF;Huppa, JB;Ploegh, HL
小鼠巨细胞病毒(MCMV)通过在内质网(ER)中保留主要组织相容性复合体(MHC)I类分子来干扰抗原提呈。在这里，我们鉴定并鉴定了一种MCMV编码的糖蛋白gp34，它与内质网中适当构象的MHC I类分子紧密结合。Gp34在MCMV感染过程中大量合成，使内质网仅与MHC I类复合体结合。在MCMV感染的早期阶段，许多但不是所有的I类分子保留在内质网中，我们观察到感染过程中合成的gp34数量与I类保留之间存在负相关。缺少几个基因的MCMV缺失突变体，包括编码gp34的基因，显示出I类保留率增加。因此，MCMV gp34可能会抵消I类保留，可能是为了降低感染细胞对自然杀伤细胞识别的敏感性。
Murine cytomegalovirus (MCMV) interferes with antigen presentation by means of retaining major histocompatibility complex (MHC) class I molecules in the endoplasmic reticulum (ER). Here we identify and characterize an MCMV-encoded glycoprotein, gp34, which tightly associates with properly conformed MHC class I molecules in the ER. Gp34 is synthesized in large quantities during MCMV infection and it leaves the ER only in association with MHC class I complexes. Many but not all class I molecules are retained in the ER during the early phase of MCMV infection, and we observe an inverse correlation between amounts of gp34 synthesized during the course of infection and class I retention. An MCMV deletion mutant lacking several genes, including the gene encoding gp34, shows increased class I retention. Thus, MCMV gp34 may counteract class I retention, perhaps to decrease susceptibility of infected cells to recognition by natural killer cells.