Reactive oxygen species regulate activation-induced T cell apoptosis
Reactive oxygen species regulate activation-induced T cell apoptosis
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DOI：
10.1016/s1074-7613(00)80072-2
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发表时间：
1999-06-01
期刊：
影响因子：
32.4
通讯作者：
Marrack, PC
中科院分区：
文献类型：
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作者：
Hildeman, DA;Mitchell, T;Marrack, PC
活性氧（ROS）在许多细胞类型中介导凋亡。我们通过体内活化T细胞，然后短时间培养，研究了ROS在活化T细胞凋亡中的作用。活化的T细胞死亡独立于Fas和TNF α。其死亡的特征是线粒体跨膜电位（Δ psi（m）），半胱天冬酶依赖的DNA片段化和超氧化物的产生的快速损失。超氧化物歧化酶模拟物Mn（III）四（5，10，15，20-苯甲酸）卟啉（MnTBAP）保护T细胞免于超氧化物生成、半胱天冬酶依赖性DNA损失、Δ psi（m）损失和细胞死亡。这些结果表明，ROS可以调节参与caspase激活和凋亡的信号，并可能有助于外周T细胞缺失。
Reactive oxygen species (ROS) mediate apoptosis in a number of cell types. We studied the role that ROS play in activated T cell apoptosis by activating T cells in vivo and then culturing them for a short time. Activated T cells died independently of Fas and TNF alpha. Their death was characterized by rapid loss of mitochondrial transmembrane potential (Delta psi(m)), caspase-dependent DNA fragmentation, and superoxide generation. A superoxide dismutase mimetic, Mn (III) tetrakis (5, 10, 15, 20-benzoic acid) porphyrin (MnTBAP), protected T cells from superoxide generation, caspase-dependent DNA loss, loss of Delta psi(m), and cell death. These results indicate that ROS can regulate signals involved in caspase activation and apoptosis and may contribute to peripheral T cell deletion.