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APO-1/Fas(CD95)介导的细胞凋亡在免疫耐受和艾滋病中的分子机制

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

作者信息

Dhein J, Walczak H, Westendorp M O, Bäumler C, Stricker K, Frank R, Debatin K M, Krammer P H

机构信息

Tumorimmunology Program, German Cancer Research Center, Heidelberg.

出版信息

Behring Inst Mitt. 1995 Jun(96):13-20.

PMID:7575348
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.

摘要

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,在被激动性抗体或其配体交联后介导细胞凋亡。最近的研究结果表明,APO-1/Fas(CD95)及其配体是活化成熟T细胞中抗原受体诱导细胞凋亡的关键分子。在此,我们提出一种通过APO-1配体介导的自分泌自杀作用导致活化T细胞抗原受体诱导细胞凋亡的机制。这一机制可能也与艾滋病中CD4+T细胞的耗竭有关。

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