STING in tumor and host cells cooperatively work for NK cell-mediated tumor growth retardation
STING in tumor and host cells cooperatively work for NK cell-mediated tumor growth retardation
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DOI：
10.1016/j.bbrc.2016.09.021
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发表时间：
2016-09-30
影响因子：
3.1
通讯作者：
Seya, Tsukasa
中科院分区：
文献类型：
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作者：
Takashima, Ken;Takeda, Yohei;Seya, Tsukasa
干扰素诱导的DNA传感器STING参与小鼠模型的肿瘤排斥反应。在这里，我们研究了NK细胞在体内导致sting依赖性B16黑色素瘤亚群生长迟缓的机制。研究使用WT和STING KO黑鼠，以及为本研究建立的B16D8（一种具有STING的nk敏感黑色素瘤系）和STING KO B16D8亚系。肿瘤植入研究结果表明，宿主免疫细胞和肿瘤细胞中的STING诱导了不同类型的趋化因子，包括CXCL10、CCL5和IL-33，这些趋化因子都参与了B16D8肿瘤的NI（细胞浸润和活化）。这种nk敏感肿瘤的宿主免疫细胞和肿瘤细胞自发激活STING，从而抑制B16D8肿瘤的生长。我们的数据表明，STING通过肿瘤和宿主免疫细胞网络诱导NK细胞的肿瘤细胞毒性，有助于体内肿瘤的先天监视和抑制。(C) 2016 Elsevier Inc.版权所有。
An interferon-inducing DNA sensor STING participates in tumor rejection in mouse models. Here we examined what mechanisms contribute to STING-dependent growth retardation of B16 melanoma sublines by NK cells in vivo. The studies were designed using WT and STING KO black mice, and B16D8 (an NK-sensitive melanoma line having STING) and STING KO B16D8 sublines established for this study. The results from tumor-implant studies suggested that STING in host immune cells and tumor cells induced distinct profiles of chemokines including CXCL10, CCL5 and IL-33, and both participated in NI( cell infiltration and activation in B16D8 tumor. Spontaneous activation of STING occurs in host-immune and tumor cells of this NK-sensitive tumor, thereby B16D8 tumor growth being suppressed in this model. Our data show that STING induces tumor cytotoxicity by NK cells through tumor and host immune cell network to contribute to innate surveillance and suppression of tumors in vivo. (C) 2016 Elsevier Inc. All rights reserved.