T细胞受体
CD3型
生物
CD8型
T细胞
细胞生物学
程序性细胞死亡
分子生物学
DNA断裂
细胞凋亡
细胞毒性T细胞
信号转导
免疫系统
免疫学
生物化学
体外
作者
Ottmar Janßen,Sebastian Wesselborg,Brigitte Heckl‐Östreicher,Klaus Pechhold,Axel Bender,S Schondelmaier,G Moldenhauer,Dieter Kabelitz
出处
期刊:Journal of Immunology
[The American Association of Immunologists]
日期:1991-01-01
卷期号:146 (1): 35-39
被引量:166
标识
DOI:10.4049/jimmunol.146.1.35
摘要
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.
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