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免疫刺激型CpG寡核苷酸可使慢性淋巴细胞白血病B细胞发生增殖、产生细胞因子并呈现免疫原性表型。

Immunostimulatory CpG-oligonucleotides cause proliferation, cytokine production, and an immunogenic phenotype in chronic lymphocytic leukemia B cells.

作者信息

Decker T, Schneller F, Sparwasser T, Tretter T, Lipford G B, Wagner H, Peschel C

机构信息

IIIrd Department of Medicine and the Institute of Medical Microbiology and Hygiene, Technical University of Munich, Munich, Germany.

出版信息

Blood. 2000 Feb 1;95(3):999-1006.

Abstract

Bacterial DNA and synthetic CpG-oligodeoxynucleotides (ODNs) derived thereof have attracted attention because they activate cells of the immune system in a sequence-dependent manner. Here we investigated the potential of CpG-ODNs to cause proliferation, cytokine production, and regulation of surface molecules in human B-chronic lymphocytic leukemia (CLL) cells. CpG-ODN induced proliferation in both B-CLL cells and normal B cells; however, only B-CLL cells increased proliferative responses when CpG-ODN was added to co-cultures of CD40-ligand transfected mouse fibroblasts (CD40LF) and B cells. Production of interleukin-6 and tumor necrosis factor alpha was detectable at borderline levels, using CpG-ODN as the only stimulus. In contrast, when CpG-ODN was added to co-cultures of B cells and CD40LF, a strong increase in cytokine production occurred in B-CLL cells as well as in normal B cells. The surface molecules CD40, CD58, CD80, CD86, CD54, and MHC class I molecules were up-regulated in B-CLL cells, whereas CD95 expression was not influenced by CpG-ODN stimulation. The same pattern of surface molecule regulation was observed in normal B cells, but up-regulation of CD40 was significantly stronger in B-CLL cells. Costimulation with CpG-ODN and CD40LF resulted in further up-regulation of CD58, CD80, CD86, and MHC class I molecules. In contrast, CD95 expression induced by CD40-ligation was inhibited by CpG-ODN. CpG-ODN activated B-CLL cells acquired a strong stimulatory capacity toward T cells in allogeneic mixed lymphocyte reaction. This effect was completely inhibited by a combination of anti-CD80 and anti-CD86 monoclonal antibody. Taken together, these findings suggest the possible use of CpG-ODN for immunotherapeutic strategies in patients with B-CLL.

摘要

细菌DNA及其衍生的合成CpG-寡脱氧核苷酸(ODN)因其以序列依赖的方式激活免疫系统细胞而备受关注。在此,我们研究了CpG-ODN在人B细胞慢性淋巴细胞白血病(CLL)细胞中引起增殖、细胞因子产生及表面分子调节的潜力。CpG-ODN可诱导B-CLL细胞和正常B细胞增殖;然而,仅当将CpG-ODN添加到CD40配体转染的小鼠成纤维细胞(CD40LF)与B细胞的共培养物中时,B-CLL细胞的增殖反应才会增强。以CpG-ODN作为唯一刺激时,可检测到白细胞介素-6和肿瘤坏死因子α的产生处于临界水平。相反,当将CpG-ODN添加到B细胞与CD40LF的共培养物中时,B-CLL细胞以及正常B细胞中的细胞因子产生均显著增加。B-CLL细胞中表面分子CD40、CD58、CD80、CD86、CD54和MHC I类分子上调,而CD95表达不受CpG-ODN刺激的影响。在正常B细胞中也观察到相同的表面分子调节模式,但B-CLL细胞中CD40的上调明显更强。CpG-ODN与CD40LF共刺激导致CD58、CD80、CD86和MHC I类分子进一步上调。相反,CD40连接诱导的CD95表达受到CpG-ODN的抑制。经CpG-ODN激活的B-CLL细胞在同种异体混合淋巴细胞反应中对T细胞获得了强大的刺激能力。抗CD80和抗CD86单克隆抗体的联合使用可完全抑制此效应。综上所述,这些发现提示CpG-ODN可能用于B-CLL患者的免疫治疗策略。

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