T cells express a phagocyte-type NADPH oxidase that is activated after T cell receptor stimulation
T cells express a phagocyte-type NADPH oxidase that is activated after T cell receptor stimulation
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DOI：
10.1038/ni1096
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发表时间：
2004-08-01
影响因子：
30.5
通讯作者：
Williams, MS
中科院分区：
文献类型：
--
作者：
Jackson, SH;Devadas, S;Williams, MS
T细胞受体（TCR）刺激可诱导活性氧物质快速产生，尽管其机制尚不清楚。在此我们发现T细胞表达一种有功能的吞噬细胞型烟酰胺腺嘌呤二核苷酸磷酸（NADPH）氧化酶。TCR交联通过募集预先形成的Fas配体和Fas诱导氧化酶活化。TCR刺激诱导产生活性氧物质的三个可区分的事件：不依赖Fas或NADPH氧化酶的快速过氧化氢产生；依赖Fas和NADPH氧化酶的持续过氧化氢产生；以及依赖Fas配体和Fas但不依赖NADPH氧化酶的延迟超氧化物产生。NADPH氧化酶缺陷型T细胞显示激酶Erk活化增强以及1型辅助性T细胞（Th1）细胞因子分泌相对增加。因此，成熟T细胞表达一种吞噬细胞型NADPH氧化酶，其调节TCR信号传导的要素。
T cell receptor (TCR) stimulation induces rapid generation of reactive oxygen species, although the mechanisms for this are unclear. Here we found that T cells expressed a functional phagocyte-type nicotinamide adenine dinucleotide phosphate (NADPH) oxidase. TCR crosslinking induced oxidase activation through the recruitment of preformed Fas ligand and Fas. TCR stimulation induced three separable events generating reactive oxygen species: rapid hydrogen peroxide production independent of Fas or NADPH oxidase; sustained hydrogen peroxide production dependent on both Fas and NADPH oxidase; and delayed superoxide production that was dependent on Fas ligand and Fas yet independent of NADPH oxidase. NADPH oxidase-deficient T cells showed enhanced activation of the kinase Erk and a relative increase in T helper type 1 cytokine secretion. Thus, mature T cells express a phagocyte-type NADPH oxidase that regulates elements of TCR signaling.