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本文引用的文献

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Matrix metalloproteinases: regulators of the tumor microenvironment.基质金属蛋白酶:肿瘤微环境的调节剂。
Cell. 2010 Apr 2;141(1):52-67. doi: 10.1016/j.cell.2010.03.015.
2
Contribution of MyD88 to the tumor exosome-mediated induction of myeloid derived suppressor cells.MyD88 对肿瘤外泌体介导的髓系来源抑制细胞诱导作用的贡献。
Am J Pathol. 2010 May;176(5):2490-9. doi: 10.2353/ajpath.2010.090777. Epub 2010 Mar 26.
3
Membrane-associated Hsp72 from tumor-derived exosomes mediates STAT3-dependent immunosuppressive function of mouse and human myeloid-derived suppressor cells.肿瘤来源的外泌体中膜相关的 HSP72 通过 STAT3 介导小鼠和人源髓系来源抑制细胞的免疫抑制功能。
J Clin Invest. 2010 Feb;120(2):457-71. doi: 10.1172/JCI40483. Epub 2010 Jan 19.
4
Myeloid-derived suppressor cells inhibit T-cell activation by depleting cystine and cysteine.髓源性抑制细胞通过耗竭半胱氨酸和胱氨酸来抑制 T 细胞的活化。
Cancer Res. 2010 Jan 1;70(1):68-77. doi: 10.1158/0008-5472.CAN-09-2587. Epub 2009 Dec 22.
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Microenvironmental pH is a key factor for exosome traffic in tumor cells.微环境pH值是肿瘤细胞中外泌体运输的关键因素。
J Biol Chem. 2009 Dec 4;284(49):34211-22. doi: 10.1074/jbc.M109.041152. Epub 2009 Sep 30.
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Tumor apoptotic bodies inhibit CTL responses and antitumor immunity via membrane-bound transforming growth factor-beta1 inducing CD8+ T-cell anergy and CD4+ Tr1 cell responses.肿瘤凋亡小体通过膜结合转化生长因子-β1诱导CD8 + T细胞无反应性和CD4 + Tr1细胞反应,从而抑制CTL反应和抗肿瘤免疫。
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Membrane-bound HSP70-engineered myeloma cell-derived exosomes stimulate more efficient CD8(+) CTL- and NK-mediated antitumour immunity than exosomes released from heat-shocked tumour cells expressing cytoplasmic HSP70.膜结合 HSP70 工程骨髓瘤细胞衍生的外泌体比表达细胞质 HSP70 的热休克肿瘤细胞释放的外泌体更能刺激有效的 CD8(+)CTL 和 NK 介导的抗肿瘤免疫。
J Cell Mol Med. 2010 Nov;14(11):2655-66. doi: 10.1111/j.1582-4934.2009.00851.x.
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Membrane vesicles as conveyors of immune responses.膜囊泡作为免疫反应的传递者。
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9
Induction of myeloid-derived suppressor cells by tumor exosomes.肿瘤外泌体诱导髓源性抑制细胞
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Myeloid-derived suppressor cells as regulators of the immune system.髓源性抑制细胞作为免疫系统的调节因子。
Nat Rev Immunol. 2009 Mar;9(3):162-74. doi: 10.1038/nri2506.

TLR2 介导的 MDSCs 扩增依赖于肿瘤外泌体的来源。

TLR2-mediated expansion of MDSCs is dependent on the source of tumor exosomes.

机构信息

Department of Microbiology & Immunology, JamesBrown Cancer Center, University of Louisville, Louisville, Kentucky 40202, USA.

出版信息

Am J Pathol. 2010 Oct;177(4):1606-10. doi: 10.2353/ajpath.2010.100245. Epub 2010 Aug 27.

DOI:10.2353/ajpath.2010.100245
PMID:20802178
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2947257/
Abstract

Exosomes released from tumor cells having been shown to induce interleukin-6 release from myeloid-derived suppressor cells in a Toll-like receptor 2/Stat3-dependent manner. In this study, we show that exosomes released from tumor cells re-isolated from syngeneic mice are capable of inducing interleukin-6 in a Toll-like receptor 2-independent manner, whereas the data generated from exosomes of tumor cells having undergone numerous in vitro passages induce interleukin-6 in a Toll-like receptor 2-dependent manner. This discrepancy may be due to the source of tumor cells used to generate the exosomes for this study. These results suggest that exosomes released from tumor cells that are not within a tumor microenvironment may not realistically represent the role of tumor exosomes in vivo. This is an important consideration since frequently passing tumor cells in vivo is an accepted practice for studying tumor exosome-mediated inflammatory responses.

摘要

已证实肿瘤细胞释放的外泌体能够通过 Toll 样受体 2/Stat3 依赖性方式诱导髓源抑制细胞释放白细胞介素-6。在这项研究中,我们表明,从同种小鼠中重新分离的肿瘤细胞释放的外泌体能够以 Toll 样受体 2 非依赖性方式诱导白细胞介素-6,而来自经历了多次体外传代的肿瘤细胞的外泌体则以 Toll 样受体 2 依赖性方式诱导白细胞介素-6。这种差异可能是由于用于生成本研究中外泌体的肿瘤细胞来源不同。这些结果表明,来自肿瘤微环境之外的肿瘤细胞释放的外泌体可能无法真实地代表肿瘤外泌体在体内的作用。这是一个重要的考虑因素,因为经常在体内传递肿瘤细胞是研究肿瘤外泌体介导的炎症反应的一种被接受的做法。