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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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Molecular mechanisms of APO-1/Fas(CD95)-mediated apoptosis in tolerance and AIDS.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
Behring Inst Mitt. 1995 Jun(96):13-20.
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Autocrine T-cell suicide mediated by APO-1/(Fas/CD95).由APO-1/(Fas/CD95)介导的自分泌T细胞自杀
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Immune down-regulation and peripheral deletion of CD8 T cells does not require TNF receptor-ligand interactions nor CD95 (Fas, APO-1).CD8 T细胞的免疫下调和外周缺失既不需要肿瘤坏死因子受体-配体相互作用,也不需要CD95(Fas,APO-1)。
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Thyroid carcinoma cells are resistant to FAS-mediated apoptosis but sensitive to tumor necrosis factor-related apoptosis-inducing ligand.甲状腺癌细胞对FAS介导的凋亡具有抗性,但对肿瘤坏死因子相关凋亡诱导配体敏感。
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Autoimmune disease results from multiple interactive defects in apoptosis induction molecules and signaling pathways.自身免疫性疾病是由凋亡诱导分子和信号通路中的多种相互作用缺陷引起的。
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Stromal derived factor-1 alpha (SDF-1 alpha) induces CD4+ T cell apoptosis via the functional up-regulation of the Fas (CD95)/Fas ligand (CD95L) pathway.基质衍生因子-1α(SDF-1α)通过Fas(CD95)/Fas配体(CD95L)途径的功能上调诱导CD4+T细胞凋亡。
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