Human immunodeficiency virus (HIV) type 1 Vpr induces differential regulation of T cell costimulatory molecules: direct effect of Vpr on T cell activation and immune function.
Human immunodeficiency virus (HIV) type 1 Vpr induces differential regulation of T cell costimulatory molecules: direct effect of Vpr on T cell activation and immune function.
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人类免疫缺陷病毒 (HIV) 1 型 Vpr 诱导 T 细胞共刺激分子的差异调节：Vpr 对 T 细胞激活和免疫功能的直接影响。
DOI：
10.1016/j.virol.2006.08.030
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发表时间：
2007
期刊：
影响因子：
3.7
通讯作者：
Ayyavoo,Velpandi
中科院分区：
文献类型：
--
作者：
Venkatachari,NarasimhanJ;Majumder,Biswanath;Ayyavoo,Velpandi
人类免疫缺陷病毒1型（HIV-1）病毒蛋白破坏正常的宿主细胞免疫途径，从而利用细胞机制进行复制、存活和逃避宿主免疫攻击。在这里，我们评估了HIV-1 Vpr介导的受感染T细胞免疫调节的直接影响。Vpr特异性下调CD 28表达，上调CTLA-4表达，而CD 25和HLA-DR表达无明显差异。评价T细胞中干扰素γ（IFN-γ）的产生，作为下游效应子功能的量度。结果表明Vpr显著抑制IFN-γ的产生，这可能部分归因于Vpr抑制NF-κB核转位及其转录调节的能力。这些结果共同支持HIV-1 Vpr在多个水平选择性地失调免疫功能，并在其他病毒蛋白存在下发挥其抑制作用。
Human immunodeficiency virus type 1 (HIV-1) viral proteins disrupt the normal host cellular immune pathways thus exploiting the cellular machinery for replication, survival and to escape host immune attack. Here we evaluated the direct effects of HIV-1 Vpr-mediated immune modulation of infected T cells. Vpr specifically downregulated the expression of CD28 and increased the expression of CTLA-4, whereas no significant difference in the expression of CD25 and HLA-DR was observed. Interferon gamma (IFN-γ) production in T cells was evaluated as a measure of the downstream effector functions. Results indicate that Vpr significantly inhibited IFN-γ production and this may, in part, due to Vpr's ability to inhibit the nuclear translocation of NF-κB, and its transcriptional regulation. Together these results support that HIV-1 Vpr selectively dysregulates the immune functions at multiple levels and exerts its inhibitory effects in the presence of other viral proteins.