首页> 美国卫生研究院文献>Proceedings of the National Academy of Sciences of the United States of America >Antigen-liposome modification of target cells as a method to alter their susceptibility to lysis by cytotoxic T lymphocytes.
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Antigen-liposome modification of target cells as a method to alter their susceptibility to lysis by cytotoxic T lymphocytes.

机译:对靶细胞进行抗原脂质体修饰以改变其对细胞毒性T淋巴细胞裂解的敏感性。

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摘要

A method of liposome modification of cell surfaces to render unsuitable target cells susceptible to lysis by anti-viral cytotoxic T lymphocytes (CTLs) is described. Liposomes containing the hemagglutinin-neuraminidase (HN) and fusion (F) glycoproteins of Sendai virus as well as purified H-2Kk cells and rendering those cells susceptible to lysis by B10. A anti-Sendai virus or anti-H-2Kk CTLs. The absence from the modifying liposomes of the HN or F proteins or H-2Kk antigens eliminated the ability of the target cells to be recognized and lysed by either effector cell population. Vesicles containing HN, H-2Kk molecules, and inactive fusion protein (Fo) were not capable of increasing the susceptibility of h-2-negative target cells to lysis. Liposomes containing inactive fusion protein were similarly unable to render H-2-positive target cells susceptible to lysis by anti-Sendai virus CTLs, suggesting that fusion of the liposomes to the cell surface is a prerequisite to lysis. It did not appear that attachement of liposomes to the cell surface was sufficient for generation of susceptible targets, however, because attachment to the cell surface was observed, as long as the HN glycoprotein was present in the liposomes. These results indicate that purified H-2Kk glycoproteins are target antigens for anti-H-2k CTLs and that B10 . A anti-Sendai virus CTLs recognize in an H-2-restricted manner the HN, F, or both glycoproteins of Sendai virus in the context of the purified H-2Kk glycoproteins. This technique of liposome modification of cell surfaces has potential applications in the examination of CTL antigen recognition and immunotherapy of many viral and neoplastic diseases.
机译:描述了脂质体修饰细胞表面以使不合适的靶细胞易于被抗病毒细胞毒性T淋巴细胞(CTL)裂解的方法。脂质体含有仙台病毒的血凝素神经氨酸酶(HN)和融合(F)糖蛋白,以及纯化的H-2Kk细胞,并使这些细胞易于被B10裂解。抗仙台病毒或抗H-2Kk CTL。 HN或F蛋白或H-2Kk抗原的修饰脂质体的缺乏消除了靶细胞被任一效应细胞群体识别和裂解的能力。包含HN,H-2Kk分子和非活性融合蛋白(Fo)的囊泡不能增加h-2-阴性靶细胞裂解的敏感性。含有无活性融合蛋白的脂质体同样不能使H-2阳性靶细胞易于被抗仙台病毒CTL裂解,这表明脂质体与细胞表面融合是裂解的先决条件。似乎脂质体与细胞表面的附着不足以产生易感靶标,但是,因为只要脂质体中存在HN糖蛋白,就可以观察到与细胞表面的附着。这些结果表明,纯化的H-2Kk糖蛋白是抗H-2k CTL的靶抗原,并且是B10。在纯化的H-2Kk糖蛋白的背景下,抗仙台病毒CTL以H-2限制性方式识别仙台病毒的HN,F或两种糖蛋白。这种对细胞表面进行脂质体修饰的技术在检查CTL抗原识别和许多病毒性和肿瘤性疾病的免疫疗法中具有潜在的应用。

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