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针对抗原处理缺陷型RMA - S肿瘤细胞系的细胞毒性T淋巴细胞。

Cytotoxic T lymphocytes against the antigen-processing-defective RMA-S tumor cell line.

作者信息

Sijts A J, De Bruijn M L, Nieland J D, Kast W M, Melief C J

机构信息

Division of Immunohematology and Bloodbank, Academic Hospital Leiden, The Netherlands.

出版信息

Eur J Immunol. 1992 Jun;22(6):1639-42. doi: 10.1002/eji.1830220644.

Abstract

RMA-S is an antigen processing-defective cell line, obtained from a Rauscher virus-induced tumor. The cells express only a low level of cell surface major histocompatibility complex (MHC) class I molecules, which are supposed to be devoid of internally derived antigenic peptides. We investigated Rauscher virus expression and Rauscher peptide presentation to virus-specific cytotoxic T lymphocytes (CTL) by this cell line. Viral proteins are expressed properly, both intracellularly and at the cell surface of RMA-S. Rauscher peptides are presented to virus-specific CTL in the groove of both the class I H-2Kb and Db molecules, but at a low level. Culture of RMA-S cells at room temperature increases their susceptibility to CTL. The RMA-S defect thus affects, but not totally abrogates, Rauscher peptide presentation by MHC class I molecules via the endogenous pathway. This indicates that the RMA-S antigen processing deficit is not absolute.

摘要

RMA-S是一种抗原处理缺陷型细胞系,源自劳氏肉瘤病毒诱导的肿瘤。这些细胞仅表达低水平的细胞表面主要组织相容性复合体(MHC)I类分子,据推测这些分子缺乏内源性抗原肽。我们研究了该细胞系中劳氏肉瘤病毒的表达以及劳氏肉瘤肽向病毒特异性细胞毒性T淋巴细胞(CTL)的呈递情况。病毒蛋白在RMA-S细胞内和细胞表面均能正常表达。劳氏肉瘤肽在I类H-2Kb和Db分子的凹槽中呈递给病毒特异性CTL,但呈递水平较低。在室温下培养RMA-S细胞会增加它们对CTL的敏感性。因此,RMA-S缺陷影响但并未完全消除MHC I类分子通过内源性途径呈递劳氏肉瘤肽的过程。这表明RMA-S的抗原处理缺陷并非绝对。

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