Molecular mechanisms of APO-1/Fas(CD95)-mediated apoptosis in tolerance and AIDS.

Behring Institute Mitteilungen Pub Date : 1995-06-01
J Dhein, H Walczak, M O Westendorp, C Bäumler, K Stricker, R Frank, K M Debatin, P H Krammer
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引用次数: 0

Abstract

The cell surface molecule APO-1/Fas(CD95), a member of the Tumor Necrosis Factor (TNF) receptor/Nerve Growth Factor (NGF) receptor superfamily mediates apoptosis upon cross-linking by agonistic antibodies or its ligand. Recent findings suggest that APO-1/Fas(CD95) and its ligand are the key molecules for antigen receptor-induced apoptosis in activated mature T cells. Here we propose a mechanism for antigen receptor-induced apoptosis of activated T cells via APO-1 ligand mediated autocrine suicide. This mechanism may also contribute to the depletion of CD4+ T cells in AIDS.

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APO-1/Fas(CD95)介导的细胞凋亡在耐受性和艾滋病中的分子机制。
细胞表面分子APO-1/Fas(CD95)是肿瘤坏死因子(TNF)受体/神经生长因子(NGF)受体超家族的成员,通过激动抗体或其配体交联介导细胞凋亡。最近的研究表明,APO-1/Fas(CD95)及其配体是激活的成熟T细胞中抗原受体诱导的凋亡的关键分子。在这里,我们提出了抗原受体通过APO-1配体介导的自分泌自杀诱导活化T细胞凋亡的机制。这一机制也可能导致艾滋病中CD4+ T细胞的耗竭。
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