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表达Fas配体的肿瘤外泌体介导CD8+ T细胞凋亡。

Tumor exosomes expressing Fas ligand mediate CD8+ T-cell apoptosis.

作者信息

Abusamra Ashraf J, Zhong Zhaohui, Zheng Xiufen, Li Mu, Ichim Thomas E, Chin Joseph L, Min Wei-Ping

机构信息

London Health Science Centers, London, Ontario, Canada.

出版信息

Blood Cells Mol Dis. 2005 Sep-Oct;35(2):169-73. doi: 10.1016/j.bcmd.2005.07.001.

DOI:10.1016/j.bcmd.2005.07.001
PMID:16081306
Abstract

Tumor-derived immune suppression is considered to be a major mechanism of tumor evasion from the immune system destruction, however, little is known regarding the induction of T-cell functional suppression by tumor-derived exosomes. Herein, we investigate tumor-derived exosomes involved in normal immunological communications as means of inhibiting an antitumor T-cell response. Exosomes derived from LNCaP, a human prostate cancer cell line, were visualized by FACS and identified based on size (80-200 nm) in comparison to marker beads. Exosomes from tumor cell line inhibited T-cell proliferation. Dose-dependent apoptosis of T cells was induced by co-culture with tumor exosomes. Addition of anti-FasL antibody blocked the apoptosis induction by tumor exosomes. This study suggests that induction of T-cell apoptosis by tumor-derived exosomes appears to be a novel mechanism of tumor immune evasion.

摘要

肿瘤源性免疫抑制被认为是肿瘤逃避免疫系统破坏的主要机制,然而,关于肿瘤源性外泌体诱导T细胞功能抑制的了解却很少。在此,我们研究参与正常免疫通讯的肿瘤源性外泌体作为抑制抗肿瘤T细胞反应的手段。通过荧光激活细胞分选术(FACS)对源自人前列腺癌细胞系LNCaP的外泌体进行可视化,并根据其大小(80-200nm)与标记微珠比较进行鉴定。肿瘤细胞系来源的外泌体抑制T细胞增殖。与肿瘤外泌体共培养可诱导T细胞剂量依赖性凋亡。添加抗FasL抗体可阻断肿瘤外泌体诱导的凋亡。本研究表明,肿瘤源性外泌体诱导T细胞凋亡似乎是肿瘤免疫逃逸的一种新机制。

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