| Literature DB >> 30813924 |
Shixin Duan1,2,3, Weihua Guo1,2,3, Zuxing Xu2, Yunbo He2, Chuting Liang2, Yongzhen Mo2, Yian Wang2, Fang Xiong2, Can Guo2, Yong Li2,4, Xiaoling Li2, Guiyuan Li1,2,3, Zhaoyang Zeng1,2,3, Wei Xiong5,6,7, Fuyan Wang8,9.
Abstract
The immune system plays important roles in tumor development. According to the immune-editing theory, immune escape is the key to tumor survival, and exploring the mechanisms of tumor immune escape can provide a new basis for the treatment of tumors. In this review, we describe the mechanisms of natural killer group 2D (NKG2D) receptor and NKG2D ligand (NKG2DL) in tumor immune responses.Natural killer (NK) cells are important cytotoxic cells in the immune system, and the activated NKG2D receptor on the NK cell surface can bind to NKG2DL expressed in tumor cells, enabling NK cells to activate and kill tumor cells. However, tumors can escape the immune clearance mediated by NKG2D receptor/NKG2DL through various mechanisms. The expression of NKG2D receptor on NK cells can be regulated by cells, molecules, and hypoxia in the tumor microenvironment. Tumor cells regulate the expression of NKG2DL at the level of transcription, translation, and post-translation and thereby escape recognition by NK cells. In particular, viruses and hormones have special mechanisms to affect the expression of NKG2D receptor and NKG2DL. Therefore, NKG2D\NKG2DL may have applications as targets for more effective antitumor therapy.Entities:
Keywords: Natural killer cell; Natural killer group 2D ligand; Natural killer group 2D receptor; Tumor; Tumor escape; Tumor microenvironment
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Year: 2019 PMID: 30813924 PMCID: PMC6391774 DOI: 10.1186/s12943-019-0956-8
Source DB: PubMed Journal: Mol Cancer ISSN: 1476-4598 Impact factor: 27.401