β干扰素对从人脐带血分离的CD4 + T细胞感染人T细胞白血病病毒I型的保护作用。
Protective effect of interferon beta on human T cell leukaemia virus type I infection of CD4+ T cells isolated from human cord blood.
作者信息
Macchi B, Faraoni I, Mastino A, D'Onofrio C, Romeo G, Bonmassar E
机构信息
Department of Experimental Medicine and Biochemical Sciences, University of Rome Tor Vergata, Italy.
出版信息
Cancer Immunol Immunother. 1993 Jul;37(2):97-104. doi: 10.1007/BF01517041.
The present study shows the effect of human interferon beta (IFN beta) on the susceptibility of highly purified cord blood CD4+ T cells to infection with the human T cell leukaemia virus type I (HTLV-I). Unfractionated cord blood mononuclear cells (CBMC), or a separated CD4+ T cell subpopulation (CBCD4) were exposed to HTLV-I by cocultivation with a chronically infected virus-donor cell line. The results show that presence of proviral DNA as well as virus transcription was markedly reduced by IFN beta in both populations, indicating that this cytokine protects not only unfractionated CBMC but also purified CBCD4 cells from virus infection. Moreover IFN beta treatment caused 60%-80% inhibition of virus expression in CBCD4, assayed as the presence of virus core protein p19. This study demonstrates that IFN beta is able to inhibit HTLV-I infection of CBMC through a mechanism that does not necessarily involve cell-mediated natural or antigen-dependent immunity afforded by CBMC subpopulations distinct from targets of HTLV-I infection. Therefore it is reasonable to conclude that IFN beta has a direct protective effect on CBCD4, through induction of antiviral resistance/activity in target cells.
本研究显示了人β干扰素（IFNβ）对高度纯化的脐血CD4⁺T细胞感染I型人T细胞白血病病毒（HTLV-I）易感性的影响。将未分离的脐血单个核细胞（CBMC）或分离出的CD4⁺T细胞亚群（CBCD4）与慢性感染病毒的供体细胞系共培养，使其暴露于HTLV-I。结果表明，IFNβ使这两个群体中的前病毒DNA以及病毒转录显著减少，这表明这种细胞因子不仅保护未分离的CBMC，也保护纯化的CBCD4细胞免受病毒感染。此外，以病毒核心蛋白p19的存在作为检测指标，IFNβ处理导致CBCD4中病毒表达受到60% - 80%的抑制。本研究表明，IFNβ能够通过一种不一定涉及细胞介导的天然免疫或抗原依赖性免疫的机制抑制CBMC的HTLV-I感染，这种免疫是由不同于HTLV-I感染靶细胞的CBMC亚群提供的。因此，有理由得出结论，IFNβ通过诱导靶细胞中的抗病毒抗性/活性，对CBCD4具有直接保护作用。
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