Species-specific effects of HIV-1 Nef-mediated MHC-I downmodulation.
Species-specific effects of HIV-1 Nef-mediated MHC-I downmodulation.
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HIV-1 Nef 介导的 MHC-I 下调的物种特异性效应。
DOI：
10.1006/viro.2002.1653
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发表时间：
2002
期刊：
影响因子：
3.7
通讯作者：
Collins,KathleenL
中科院分区：
文献类型：
--
作者：
Fleis,Rebekah;Filzen,Tracey;Collins,KathleenL
体外研究表明，人类免疫缺陷病毒-1（HIV-1）Nef在功能上与主要组织相容性复合物I类（MHC-I）分子胞质尾区的氨基酸残基相互作用，降低其在细胞表面的表达，并保护其免受细胞毒性T淋巴细胞（CTL）裂解。为了更好地了解Nef在体内的作用，建立小鼠模型系统将是有益的。然而，尚不清楚Nef是否会影响鼠MHC-I蛋白。我们发现，Nef下调人类MHC-Ⅰ类HLA-A2更有效地比小鼠MHC-Ⅰ类分子在HeLa细胞和Nef不有效地在小鼠内皮细胞的功能。嵌合分子的研究表明，MHC-I胞质尾区是物种特异性差异的主要原因。然而，也存在归因于细胞外结构域的效应。
In vitro studies have revealed that human immunodeficiency virus-1 (HIV-1) Nef functionally interacts with amino acid residues in the cytoplasmic tail of major histocompatibility complex class I (MHC-I) molecules, reducing their expression on the cell surface and protecting them from cytotoxic T lymphocyte (CTL) lysis. To obtain a better understanding of Nef's effects in vivo, it would be helpful to have a mouse model system. However, it is not known whether Nef will affect murine MHC-I proteins. We find that Nef downmodulates human MHC-I HLA-A2 more efficiently than murine MHC-I molecules in HeLa cells and that Nef does not function efficiently in murine endothelial cells. Studies with chimeric molecules indicate that the MHC-I cytoplasmic tail is primarily responsible for species-specific differences. However, there are also effects attributable to the extracellular domain.