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CD40 连接可抵消 Fas 诱导的人树突状细胞凋亡。

CD40 ligation counteracts Fas-induced apoptosis of human dendritic cells.

作者信息

Björck P, Banchereau J, Flores-Romo L

机构信息

Schering-Plough Laboratory for Immunological Research, Dardilly, France.

出版信息

Int Immunol. 1997 Mar;9(3):365-72. doi: 10.1093/intimm/9.3.365.

Abstract

Dendritic cells (DC) are cells of the hematopoletic system specialized in capturing antigens and initiating T cell-mediated immune responses. We show here that human DC generated in vitro by culturing CD34+ cord blood progenitor cells in granulocyte macrophage colony stimulating factor plus tumor necrosis factor-alpha express the Fas antigen (APO-1, CD95) and undergo apoptosis upon triggering of Fas by mAb. However, only a proportion of the cells die in response to Fas ligation, an observation that may be related to the virtual absence of the bcl-2 protein in about half of the cells. Ligation of DC CD40 by culture on CD40L-transfected fibroblastic cells up-regulates the expression of bcl-2 and, concomitantly, renders DC virtually resistant to Fas-induced apoptosis. Parallel experiments with mature, interdigitating dendritic cells (IDC) isolated from tonsils revealed that IDC express Fas but do not enter into apoptosis following Fas ligation, a finding that may be explained by their high levels of bcl-2. Thus, upon encountering antigen-specific T cells, DC become resistant to Fas-induced apoptosis, as a consequence of CD40 ligation and possibly by mechanisms associated to the up-regulation of bcl-2 protein expression.

摘要

树突状细胞(DC)是造血系统中的细胞,专门负责捕获抗原并启动T细胞介导的免疫反应。我们在此表明,通过在粒细胞巨噬细胞集落刺激因子加肿瘤坏死因子-α中培养CD34 +脐血祖细胞在体外产生的人DC表达Fas抗原(APO-1,CD95),并在mAb触发Fas后发生凋亡。然而,只有一部分细胞在Fas连接时死亡,这一观察结果可能与大约一半细胞中几乎不存在bcl-2蛋白有关。通过在CD40L转染的成纤维细胞上培养来连接DC CD40会上调bcl-2的表达,并同时使DC几乎对Fas诱导的凋亡具有抗性。用从扁桃体分离的成熟、交错突树突状细胞(IDC)进行的平行实验表明,IDC表达Fas,但在Fas连接后不会发生凋亡,这一发现可能由其高水平的bcl-2来解释。因此,在遇到抗原特异性T细胞时,由于CD40连接以及可能与bcl-2蛋白表达上调相关的机制,DC对Fas诱导的凋亡产生抗性。

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