巨细胞病毒免疫逃逸的混杂性：m138/fcr-1 下调除 MULT-1 和 H60 外还下调 RAE-1epsilon。
Promiscuity of MCMV immunoevasin of NKG2D: m138/fcr-1 down-modulates RAE-1epsilon in addition to MULT-1 and H60.
机构信息
Department of Histology and Embryology, Faculty of Medicine, University of Rijeka, B. Branchetta 20, 51000 Rijeka, Croatia.
出版信息
Mol Immunol. 2009 Nov;47(1):114-22. doi: 10.1016/j.molimm.2009.02.010. Epub 2009 Mar 17.
Both human and mouse cytomegalovirus (CMV) encode proteins that inhibit the activation of NK cells by down-regulating the cellular ligands for activating NK cell receptor, NKG2D. MCMV proteins m145, m152 and m155 interfere with the expression of all known NKG2D ligands, MULT-1, RAE-1 family members and H60, respectively, whereas m138 affects the expression of MULT-1 and H60. Here we show that m152 affects the maturation of newly synthesized RAE-1 molecules, but is not sufficient to prevent surface expression of RAE-1varepsilon. We have identified m138 as a main inhibitor of the surface expression of RAE-1varepsilon. In contrast to m152, m138 affects the surface-resident protein leading to its endocytosis, which can be prevented by a dynamin inhibitor. Moreover, we demonstrated that m138 does not need other viral proteins to down-modulate the expression of RAE-1varepsilon.
人巨细胞病毒（CMV）和鼠巨细胞病毒（MCMV）均编码蛋白，通过下调 NK 细胞激活受体 NKG2D 的细胞配体来抑制 NK 细胞的激活。MCMV 蛋白 m145、m152 和 m155 分别干扰所有已知的 NKG2D 配体 MULT-1、RAE-1 家族成员和 H60 的表达，而 m138 影响 MULT-1 和 H60 的表达。在这里，我们表明 m152 影响新合成的 RAE-1 分子的成熟，但不足以阻止 RAE-1ε的表面表达。我们已经确定 m138 是 RAE-1ε表面表达的主要抑制剂。与 m152 不同，m138 影响表面驻留蛋白导致其内吞作用，该作用可以被肌球蛋白抑制剂所阻止。此外，我们证明 m138 不需要其他病毒蛋白来下调 RAE-1ε的表达。
Zotero 插件