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CD40 ligation induces Apo-1/Fas expression on human B lymphocytes and facilitates apoptosis through the Apo-1/Fas pathway

机译：CD40连接可诱导人B淋巴细胞上Apo-1 / Fas表达，并通过Apo-1 / Fas途径促进细胞凋亡

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The Apo-1/Fas antigen (CD95) mediates programmed cell death of lymphocytes when bound by Fas ligand or anti-Apo-1/Fas antibody. In contrast, the CD40 antigen provides a potent activation and survival signal to B lymphocytes when it is engaged by its T cell ligand (CD40L, gp39) or cross-linked by anti-CD40 antibody. In this study, we use human tonsillar B cells and the Ramos Burkitt's lymphoma B cell line, which serves as a model for human germinal center B lymphocytes, to study the effectors of Apo-1/Fas expression and apoptosis of human B cells. We found that Apo-1/Fas expression was upregulated on both malignant and normal human B lymphocytes after CD40 ligation induced by (a) cognate T helper-B cell interaction mediated by microbial superantigen (SAg); (b) contact-dependent interaction with CD40L+, but not CD40L- Jurkat mutant T cell clones; and (c) monoclonal anti-CD40, but not any of a panel of control antibodies. Enhanced B cell Fas/Apo-1 expression is functionally significant. Coculture of Ramos Burkitt's lymphoma line cells with irradiated SAg-reactive CD4+ T cells with SAg or CD40L+ Jurkat T cells results in B cell apoptosis, evidenced by reduced cell viability and DNA laddering. This process is augmented by the addition of anti-Apo-1/Fas monoclonal antibody, consistent with an acquired susceptibility to Apo-1/Fas-mediated apoptosis. These data support an immunoregulatory pathway in which seemingly contradictory signals involving the B cell proliferation/survival antigen CD40, as well as the Apo-1/Fas molecule, which mediates programmed cell death of lymphocytes, are linked in the process of human B cell activation.
机译：当与Fas配体或抗Apo-1 / Fas抗体结合时，Apo-1 / Fas抗原（CD95）介导淋巴细胞的程序性细胞死亡。相反，当CD40抗原被其T细胞配体（CD40L，gp39）接合或被抗CD40抗体交联时，它会向B淋巴细胞提供有效的激活和存活信号。在这项研究中，我们使用人类扁桃体B细胞和Ramos Burkitt淋巴瘤B细胞系（作为人类生发中心B淋巴细胞的模型）来研究Apo-1 / Fas表达和人类B细胞凋亡的效应。我们发现，由（a）微生物超抗原（SAg）介导的同源T辅助B细胞相互作用诱导的CD40连接后，Apo-1 / Fas表达在恶性和正常人B淋巴细胞上均上调。 （b）与CD40L +的接触依赖性相互作用，但与CD40L- Jurkat突变T细胞克隆无关。 （c）单克隆抗CD40，但没有一组对照抗体。增强的B细胞Fas / Apo-1表达在功能上很重要。将Ramos Burkitt淋巴瘤系细胞与经辐照的SAg反应性CD4 + T细胞与SAg或CD40L + Jurkat T细胞共培养会导致B细胞凋亡，这可通过降低细胞活力和DNA阶梯化来证明。通过添加抗Apo-1 / Fas单克隆抗体来增强该过程，这与获得的对Apo-1 / Fas介导的细胞凋亡的敏感性相一致。这些数据支持了一种免疫调节途径，其中涉及B细胞增殖/存活抗原CD40以及介导淋巴细胞程序性细胞死亡的Apo-1 / Fas分子的似乎矛盾的信号在人类B细胞活化过程中相互关联。

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