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首页> 外文期刊>Nature immunology >Ligand-independent redistribution of Fas (CD95) into lipid rafts mediates clonotypic T cell death
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Ligand-independent redistribution of Fas (CD95) into lipid rafts mediates clonotypic T cell death

机译:Fas(CD95)的非配体依赖性重新分布到脂质筏中,介导克隆型T细胞死亡

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摘要

Clonotypic elimination of activated T cells through Fas-Fas ligand (CD95-CD95L) interactions is one mechanism of peripheral self-tolerance. T cell receptor (TCR) stimuli trigger FasL synthesis but also sensitize activated T cells to Fas-mediated apoptosis through an unknown mechanism. Here we show that TCR restimulation of activated human CD4~+ T cells resulted in Fas translocation into lipid raft microdomains before binding FasL, rendering these cells sensitive to apoptosis after stimulation with bivalent antibody or FasL. Disruption of lipid rafts reduced sensitivity to Fas-mediated apoptosis after TCR restimulation. Thus, the redistribution of Fas and other tumor necrosis factor family receptors into and out of lipid rafts may dynamically regulate the efficiency and outcomes of signaling by these receptors.
机译:通过Fas-Fas配体(CD95-CD95L)相互作用对活化的T细胞进行克隆型消除是外周自我耐受的机制之一。 T细胞受体(TCR)刺激触发FasL合成,但也通过未知机制使活化的T细胞对Fas介导的细胞凋亡敏感。在这里,我们显示激活的人CD4〜+ T细胞的TCR重新刺激导致Fas在结合FasL之前易位到脂质筏微结构域,使这些细胞对二价抗体或FasL刺激后对凋亡敏感。脂质筏的破坏降低了TCR再刺激后对Fas介导的细胞凋亡的敏感性。因此,Fas和其他肿瘤坏死因子家族受体在脂质筏中的重新分布可能动态调节这些受体的信号传导效率和结果。

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