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Prostate Tumor-Derived Exosomes Down-Regulate NKG2D Expression on Natural Killer Cells and CD8+ T Cells: Mechanism of Immune Evasion

机译：前列腺肿瘤衍生的外泌体下调NKK2D在自然杀伤细胞和CD8 + T细胞上的表达：免疫逃逸的机制。

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Tumor-derived exosomes, which are nanometer-sized extracellular vesicles of endosomal origin, have emerged as promoters of tumor immune evasion but their role in prostate cancer (PC) progression is poorly understood. In this study, we investigated the ability of prostate tumor-derived exosomes to downregulate NKG2D expression on natural killer (NK) and CD8+ T cells. NKG2D is an activating cytotoxicity receptor whose aberrant loss in cancer plays an important role in immune suppression. Using flow cytometry, we found that exosomes produced by human PC cells express ligands for NKG2D on their surface. The NKG2D ligand-expressing prostate tumor-derived exosomes selectively induced downregulation of NKG2D on NK and CD8+ T cells in a dose-dependent manner, leading to impaired cytotoxic function in vitro. Consistent with these findings, patients with castration-resistant PC (CRPC) showed a significant decrease in surface NKG2D expression on circulating NK and CD8+ T cells compared to healthy individuals. Tumor-derived exosomes are likely involved in this NKG2D downregulation, since incubation of healthy lymphocytes with exosomes isolated from serum or plasma of CRPC patients triggered downregulation of NKG2D expression in effector lymphocytes. These data suggest prostate tumor-derived exosomes as down-regulators of the NKG2D-mediated cytotoxic response in PC patients, thus promoting immune suppression and tumor escape.
机译：肿瘤来源的外来体是内体来源的纳米大小的细胞外囊泡，已经作为肿瘤免疫逃逸的促进剂出现，但是人们对其在前列腺癌（PC）进展中的作用了解甚少。在这项研究中，我们研究了前列腺肿瘤衍生的外来体下调自然杀伤（NK）和CD8 + T细胞上NKG2D表达的能力。 NKG2D是一种活化的细胞毒性受体，其在癌症中的异常丢失在免疫抑制中起着重要作用。使用流式细胞仪，我们发现人PC细胞产生的外泌体在其表面表达NKG2D的配体。表达NKG2D配体的前列腺肿瘤来源的外来体以剂量依赖性方式选择性地诱导NK和CD8 + T细胞上NKG2D的下调，从而导致体外细胞毒性功能受损。与这些发现一致的是，与健康个体相比，去势抵抗性PC（CRPC）患者的循环NK和CD8 + T细胞表面NKG2D表达明显降低。肿瘤源性外泌体可能参与了NKG2D的下调，因为健康淋巴细胞与从CRPC患者血清或血浆中分离出的外泌体的孵育触发了效应淋巴细胞中NKG2D表达的下调。这些数据表明前列腺肿瘤衍生的外来体在PC患者中作为NKG2D介导的细胞毒性反应的下调剂，从而促进免疫抑制和肿瘤逃逸。

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