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首页> 外文期刊>Cellular immunology >RCAS1 induced by HIV-Tat is involved in the apoptosis of HIV-1 infected and uninfected CD4(+) T cells
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RCAS1 induced by HIV-Tat is involved in the apoptosis of HIV-1 infected and uninfected CD4(+) T cells

机译：HIV-Tat诱导的RCAS1参与HIV-1感染和未感染的CD4（+）T细胞的凋亡

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摘要

HIV-1 infection is known to lead to a massive depletion of CD4(+) T cells, and the Fas/FasL and TRAIL/TRAIL-receptor systems have been reported to be one of the mechanisms of CD4(+) T cell apoptosis in HIV-1 infection. RCAS1 (a receptor-binding cancer antigen expressed on SiSo cells) is also an apoptosis-associated protein that induces apoptosis in receptor positive-cells including T cells, and NK cells. To investigate the role of RCAS1 in HIV-1 infection, we stimulated CD4(+) T cells, monocytes, and several cell lines by HIV-Tat protein and thus showed that Tat significantly increased the mRNA transcription levels and the secretion of soluble RCAS1 in CD4(+) T cells and monocytes. We also showed that the apoptosis induced by HIV-Tat was blocked by inhibiting the expression of RCAS1, using small interfering RNA (siRNA), which was specific for RCAS1. These results indicate that RCAS1 is one of the mechanisms of CD4(+) T cell depletion induced by HIV infection. (c) 2007 Published by Elsevier Inc.
机译：已知HIV-1感染会导致CD4（+）T细胞大量耗竭，据报道Fas / FasL和TRAIL / TRAIL受体系统是CD4（+）T细胞凋亡的机制之一。 HIV-1感染。 RCAS1（在SiSo细胞上表达的与受体结合的癌症抗原）也是一种凋亡相关蛋白，可诱导包括T细胞和NK细胞在内的受体阳性细胞凋亡。为了研究RCAS1在HIV-1感染中的作用，我们通过HIV-Tat蛋白刺激了CD4（+）T细胞，单核细胞和几种细胞系，因此表明Tat显着增加了mRNA的转录水平和可溶性RCAS1的分泌。 CD4（+）T细胞和单核细胞。我们还表明，通过使用RCAS1特异的小干扰RNA（siRNA）抑制RCAS1的表达，可以阻止HIV-Tat诱导的细胞凋亡。这些结果表明，RCAS1是HIV感染诱导CD4（+）T细胞耗竭的机制之一。 （c）2007年由Elsevier Inc.发布。

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