Baur A, Garber S, Peterlin B M
Howard Hughes Medical Institute, University of California at San Francisco 94143-0724.
J Immunol. 1994 Feb 1;152(3):976-83.
Increased levels of replication of the HIV type 1 are observed after the activation of infected T cells through the TCR. However, anti-CD45 antibodies inhibit these effects in cells from infected individuals. In this study, we examined interrelationships between CD45 and HIV-1 further. We measured effects on the HIV-1 LTR in T cell lines that were stimulated with antibodies against CD45 and in those that lacked the expression of CD45 on their surfaces. First, anti-CD45 antibodies did not affect basal but decreased activated levels of expression from the HIV-1 LTR. Second, T cells, which lack CD45 and cannot signal via the TCR, supported higher levels of viral replication and gene expression. This was due to the presence of active NF-kappa B complexes in the nucleus of CD45- T cells. Additionally, infected T cells displayed lower levels of CD45 on their surfaces. Thus, CD45 plays an active role in the physiology of T cells and in the replication of HIV-1.
通过TCR激活受感染的T细胞后，观察到1型HIV的复制水平增加。然而，抗CD45抗体可抑制感染个体细胞中的这些效应。在本研究中，我们进一步研究了CD45与HIV-1之间的相互关系。我们在经抗CD45抗体刺激的T细胞系以及表面缺乏CD45表达的T细胞系中测量了对HIV-1 LTR的影响。首先，抗CD45抗体不影响基础水平，但可降低HIV-1 LTR的激活表达水平。其次，缺乏CD45且不能通过TCR发出信号的T细胞支持更高水平的病毒复制和基因表达。这是由于CD45-T细胞核中存在活性NF-κB复合物。此外，受感染的T细胞表面CD45水平较低。因此，CD45在T细胞生理学和HIV-1复制中发挥积极作用。
