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一个受FBL-3肿瘤细胞上的I类主要组织相容性复合体抗原限制的CD4(L3T4)阳性细胞毒性T细胞克隆的特性分析。

Characterization of a CD4(L3T4)-positive cytotoxic T cell clone that is restricted by class I major histocompatibility complex antigen on FBL-3 tumor cell.

作者信息

Matsubayashi Y, Zenita K, Morioka A, Iwashiro M, Masuda T, Uchino H, Fujita T, Kuribayashi K

机构信息

Institute of Immunology, Faculty of Medicine, Kyoto University, Japan.

出版信息

Immunobiology. 1989 Nov;180(1):33-46. doi: 10.1016/S0171-2985(89)80028-2.

Abstract

An L3T4(CD4)+ CTL clone specific for Friend virus-induced tumor FBL-3 was isolated, characterized and compared with a conventional Lyt-2(CD8)+ CTL clone. This clone L3.1 was obtained from the limiting dilution culture of splenic MLTC cells from a CB6F1 mouse whose CD8+ T cells had been suppressed by an in vivo injection of anti-Lyt-2.2 mAb. The phenotype of clone L3.1 was sIg-, Thy-1.2+, L3T4(CD4)+, Lyt-2 (CD8)-, and Ia- as determined by flow-cytometry. Northern blot analysis also confirmed that mRNA for L3T4(CD4), but not for Lyt-2 (CD8) was present in the total RNA of L3.1. The FBL-3-specific killing activity of L3.1 was inhibited by anti-H-2D6 mAb, and the tumor cells did not express class II MHC antigen, indicating that the recognition of tumor antigen by this CD4+ CTL clone was restricted by the class I MHC molecule on the tumor cells. Furthermore, the finding that anti-L3T4(CD4) mAb GK1.5 inhibited the specific and lectin-dependent non-specific cytotoxicity of L3.1 suggested that CD4 molecules on this CTL clone are not ligand (MHC class II)-binding proteins, but are involved in signal transduction.

摘要

分离出一株针对Friend病毒诱导的肿瘤FBL-3的L3T4(CD4)+ CTL克隆,对其进行了表征,并与传统的Lyt-2(CD8)+ CTL克隆进行了比较。该克隆L3.1是从一只CB6F1小鼠的脾细胞混合淋巴细胞培养物的有限稀释培养物中获得的,该小鼠的CD8+ T细胞已通过体内注射抗Lyt-2.2单克隆抗体被抑制。通过流式细胞术确定克隆L3.1的表型为sIg-、Thy-1.2+、L3T4(CD4)+、Lyt-2 (CD8)-和Ia-。Northern印迹分析也证实,L3.1的总RNA中存在L3T4(CD4)的mRNA,但不存在Lyt-2 (CD8)的mRNA。L3.1的FBL-3特异性杀伤活性被抗H-2D6单克隆抗体抑制,且肿瘤细胞不表达II类MHC抗原,这表明该CD4+ CTL克隆对肿瘤抗原的识别受肿瘤细胞上的I类MHC分子限制。此外,抗L3T4(CD4)单克隆抗体GK1.5抑制L3.1的特异性和凝集素依赖性非特异性细胞毒性这一发现表明,该CTL克隆上的CD4分子不是配体(II类MHC)结合蛋白,而是参与信号转导。

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