Edfjäll C, Jacobsen H, Lötscher H, Mous J
Pharmaceutical Research Gene Technologies, F. Hoffmann-La Roche Ltd., Basel, Switzerland.
AIDS Res Hum Retroviruses. 1996 Feb 10;12(3):199-204. doi: 10.1089/aid.1996.12.199.
Tumor necrosis factor alpha (TNF-alpha) is a potent inducer of human immunodeficiency virus type 1 (HIV-1) expression in chronically infected cells. The aim of this study was to investigate the role played by the two known TNF-alpha receptors, TNFR-p55 and TNFR-p75, in the activation of HIV-1 expression. As a model system the latently infected human promonocytic cell line U1 was stimulated with wild-type TNF-alpha, with TNF-alpha muteins that specifically bind to one or the other receptor or with receptor-specific monoclonal antibodies. Induction of HIV-1 expression, measured by p24 core antigen capture enzyme-linked immunosorbent assay (ELISA), was found to be exclusively triggered by TNFR-p55 stimulation. However, our results also showed that the addition of TNFR-p75-specific ligands negatively modulated the HIV-1 expression induced via TNFR-p55.
肿瘤坏死因子α（TNF-α）是慢性感染细胞中人类免疫缺陷病毒1型（HIV-1）表达的强效诱导剂。本研究的目的是探讨两种已知的TNF-α受体TNFR-p55和TNFR-p75在激活HIV-1表达中所起的作用。作为模型系统，用野生型TNF-α、特异性结合其中一种或另一种受体的TNF-α突变体或受体特异性单克隆抗体刺激潜伏感染的人原单核细胞系U1。通过p24核心抗原捕获酶联免疫吸附测定（ELISA）测量HIV-1表达的诱导，发现其完全由TNFR-p55刺激触发。然而，我们的结果还表明，添加TNFR-p75特异性配体可负向调节通过TNFR-p55诱导的HIV-1表达。
