Janssen O, Wesselborg S, Heckl-Ostreicher B, Pechhold K, Bender A, Schondelmaier S, Moldenhauer G, Kabelitz D
Institute of Immunology, University of Heidelberg, Federal Republic of Germany.
J Immunol. 1991 Jan 1;146(1):35-9.
mAb directed against the TCR/CD3 complex activate resting T cells. However, TCR/CD3 signaling induces death by apoptosis in immature (CD4+CD8+) murine thymocytes and certain transformed leukemic T cell lines. Here we show that anti-TCR and anti-CD3 mAb induce growth arrest of cloned TCR-gamma delta + T cells in the presence of IL-2. In the absence of exogenous IL-2, however, the very same anti-TCR/CD3 mAb stimulated gamma delta (+)-clones to proliferation and IL-2 production. In the presence of exogenous IL-2, anti-TCR/CD3 mAb induced the degradation of DNA into oligosomal bands of approximately 200 bp length in cloned gamma delta + T cells. This pattern of DNA fragmentation is characteristic for the programmed cell death termed apoptosis. These results demonstrate that TCR/CD3 signaling can induce cell death in cloned gamma delta + T cells. In addition, this report is the first to show that apoptosis triggered by TCR/CD3 signaling is not restricted to CD4+CD8+ immature thymocytes and transformed leukemic T cell lines but can be also observed with IL-2-dependent normal (i.e., TCR-gamma delta +) T cells.
针对TCR/CD3复合物的单克隆抗体可激活静息T细胞。然而，TCR/CD3信号传导可诱导未成熟（CD4 + CD8 +）小鼠胸腺细胞和某些转化的白血病T细胞系通过凋亡死亡。在此我们表明，在白细胞介素-2（IL-2）存在的情况下，抗TCR和抗CD3单克隆抗体可诱导克隆的TCR-γδ + T细胞生长停滞。然而，在没有外源性IL-2的情况下，同样的抗TCR/CD3单克隆抗体可刺激γδ（+）克隆增殖并产生IL-2。在存在外源性IL-2的情况下，抗TCR/CD3单克隆抗体可诱导克隆的γδ + T细胞中的DNA降解为长度约200 bp的寡核小体条带。这种DNA片段化模式是程序性细胞死亡即凋亡的特征。这些结果表明，TCR/CD3信号传导可诱导克隆的γδ + T细胞死亡。此外，本报告首次表明，由TCR/CD3信号传导触发的凋亡不仅限于CD4 + CD8 +未成熟胸腺细胞和转化的白血病T细胞系，在依赖IL-2的正常（即TCR-γδ +）T细胞中也可观察到。
