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肝素的抗肿瘤作用并非由直接激活自然杀伤细胞介导。

The Antitumor Effect of Heparin is not Mediated by Direct NK Cell Activation.

作者信息

Rossi Gustavo R, Gonçalves Jenifer P, McCulloch Timothy, Delconte Rebecca B, Hennessy Robert J, Huntington Nicholas D, Trindade Edvaldo S, Souza-Fonseca-Guimaraes Fernando

机构信息

Cellular Biology Department, Federal University of Paraná, Curitiba, Paraná CEP 81351-980, Brazil.

The University of Queensland Diamantina Institute, University of Queensland, Woolloongabba, QLD 4102, Australia.

出版信息

J Clin Med. 2020 Aug 18;9(8):2666. doi: 10.3390/jcm9082666.

Abstract

Natural killer (NK) cells are innate lymphocytes responsible for the elimination of infected or transformed cells. The activation or inhibition of NK cells is determined by the balance of target cell ligand recognition by stimulatory and inhibitory receptors on their surface. Previous reports have suggested that the glycosaminoglycan heparin is a ligand for the natural cytotoxicity receptors NKp30, NKp44 (human), and NKp46 (both human and mouse). However, the effects of heparin on NK cell homeostasis and function remain unclear. Here, we show that heparin does not enhance NK cell proliferation or killing through NK cell activation. Alternatively, in mice models, heparin promoted NK cell survival in vitro and controlled B16-F10 melanoma metastasis development in vivo. In human NK cells, heparin promisingly increased interferon (IFN)-γ production in synergy with IL-12, although the mechanism remains elusive. Our data showed that heparin is not able to increase NK cell cytotoxicity.

摘要

自然杀伤(NK)细胞是先天性淋巴细胞,负责清除受感染或转化的细胞。NK细胞的激活或抑制取决于其表面刺激性和抑制性受体对靶细胞配体的识别平衡。先前的报道表明,糖胺聚糖肝素是天然细胞毒性受体NKp30、NKp44(人类)和NKp46(人类和小鼠)的配体。然而,肝素对NK细胞稳态和功能的影响仍不清楚。在这里,我们表明肝素不会通过激活NK细胞来增强其增殖或杀伤能力。相反,在小鼠模型中,肝素在体外促进NK细胞存活,并在体内控制B16-F10黑色素瘤转移的发展。在人类NK细胞中,肝素有望与IL-12协同增加干扰素(IFN)-γ的产生,尽管其机制仍不清楚。我们的数据表明,肝素不能增加NK细胞的细胞毒性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f52/7463539/6c42b0bfd3cf/jcm-09-02666-g001.jpg

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