Sechoy O, Vidal M, Philippot J R, Bienvenue A
U.A. CNRS 530, INSERM U 58, Montpellier, France.
Exp Cell Res. 1989 Nov;185(1):122-31. doi: 10.1016/0014-4827(89)90042-6.
We have studied the internalization of targeted fusogenic liposome content to leukemic T cells (CEM) in vitro. We describe a method for the covalent coupling of T101 antibody to the surface of liposomes and the incorporation of fusogenic viral protein into the liposome membrane. Hygromycin B, an impermeant inhibitor of protein synthesis, was encapsulated in the targeted fusogenic liposomes and delivered directly to the cytoplasm of leukemic T cells by fusion between the two membranes. The cytotoxic effect was measured by [3H]thymidine incorporation. We show that CEM are rapidly and specifically killed by the drug encapsulated in the targeted fusogenic liposomes. This effect is due to the binding of the liposome by means of the antibody and then to the fusion of the liposome with the targeted cell membrane, mediated by F protein.
我们已经在体外研究了靶向融合脂质体内容物向白血病T细胞(CEM)的内化。我们描述了一种将T101抗体共价偶联到脂质体表面以及将融合病毒蛋白掺入脂质体膜的方法。潮霉素B是一种蛋白质合成的非渗透性抑制剂,被包封在靶向融合脂质体中,并通过两个膜之间的融合直接递送至白血病T细胞的细胞质中。通过[3H]胸苷掺入来测量细胞毒性作用。我们表明,靶向融合脂质体中包封的药物能快速且特异性地杀死CEM。这种作用是由于脂质体通过抗体结合,然后由F蛋白介导脂质体与靶细胞膜融合所致。