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首页> 外文期刊>The Journal of Experomental Medicine >CD4-CD8- T cell receptor alpha beta T cells: generation of an in vitro major histocompatibility complex class I specific cytotoxic T lymphocyte response and allogeneic tumor rejection.
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CD4-CD8- T cell receptor alpha beta T cells: generation of an in vitro major histocompatibility complex class I specific cytotoxic T lymphocyte response and allogeneic tumor rejection.

机译：CD4-CD8- T细胞受体αβT细胞：产生体外主要组织相容性复合体I类特异性细胞毒性T淋巴细胞反应和同种异体肿瘤排斥反应。

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The generation of an in vitro major histocompatibility complex class I specific response of CD4-CD8- T cell receptor (TCR) alpha beta cytotoxic T lymphocytes (CTL) and their allogeneic tumor rejection were investigated. Inocula of BALBRL male 1 were rejected in C57BL/6 (B6) mice treated with minimum essential medium (MEM) (control), anti-L3T4 (CD4) monoclonal antibody (mAb) or anti-Lyt-2.2 (CD8) mAb and CTL against the tumor were generated in vitro. No rejection and no induction of CTL were observed in B6 mice treated with anti-L3T4 (CD4) plus anti-Lyt-2.2 (CD8) mAb. CTL with the classical Thy-1+ CD3+CD4-CD8+ TCR alpha beta phenotype were generated in mixed lymphocyte tumor cell culture (MLTC) spleen cells from B6 mice treated with MEM (control) or anti-L3T4 (CD4) mAb, whereas CTL with an unusual Thy-1+CD3+CD4-CD8- TCR alpha beta phenotype were generated in MLTC spleen cells from anti-Lyt-2.2 (CD8) mAb-treated B6 mice. Both types of CTL were reactive with both H-2Kd and Dd (Ld) class I antigen. These findings suggest that when CD4+ cells were blocked by anti-L3T4 (CD4) mAb, CD8+ CTL mediated rejection, and when CD8+ cells were blocked by anti-Lyt-2.2 (CD8) mAb, CD4+ cells were capable of mediating rejection, although less efficiently than CD8+ cells, by inducing CD4-CD8- TCR alpha beta CTL. The finding that adoptive transfer of CD4 and CD8-depleted MLTC spleen cells, obtained from anti-Lyt-2.2 (CD8) mAb-treated B6 mice that had rejected BALBRL male 1, resulted in rejection of BALBRL male 1 inoculated into B6 nuu mice confirmed the above notion. CTL clones with the CD4-CD8- TCR alpha beta phenotype specific for Ld were established.
机译：研究了CD4-CD8-T细胞受体（TCR）αβ细胞毒性T淋巴细胞（CTL）的体外主要组织相容性复合体I类特异性应答的产生及其同种异体肿瘤排斥反应。在用最低必需培养基（MEM）（对照），抗L3T4（CD4）单克隆抗体（mAb）或抗Lyt-2.2（CD8）mAb和CTL处理的C57BL / 6（B6）小鼠中，BALBRL雄性1的接种被拒绝针对肿瘤是在体外产生的。在用抗L3T4（CD4）和抗Lyt-2.2（CD8）mAb处理的B6小鼠中未观察到排斥反应，也未诱导CTL。具有经典Thy-1 + CD3 + CD4-CD8 + TCRαβ表型的CTL在MEM（对照）或抗L3T4（CD4）mAb处理的B6小鼠的混合淋巴细胞肿瘤细胞培养（MLTC）脾细胞中产生，而CTL抗Lyt-2.2（CD8）mAb治疗的B6小鼠在MLTC脾细胞中产生了具有异常Thy-1 + CD3 + CD4-CD8- TCRαβ表型的细胞。两种类型的CTL都与H-2Kd和Dd（Ld）I类抗原反应。这些发现表明，当CD4 +细胞被抗L3T4（CD4）mAb阻断时，CD8 + CTL介导的排斥反应;当CD8 +细胞被抗Lyt-2.2（CD8）mAb阻断时，CD4 +细胞能够介导排斥，尽管作用较小。通过诱导CD4-CD8-TCRαβCTL，它比CD8 +细胞更有效。从抗Lyt-2.2（CD8）mAb治疗的B6小鼠（已排斥BALBRL雄性1）获得的CD4和CD8耗竭的MLTC脾细胞的过继转移发现导致接种B6 nu / nu的BALBRL雄性1的排斥小鼠证实了上述观点。建立具有对Ld特有的CD4-CD8-TCRα-β表型的CTL克隆。

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