4.6 Review

Convergent Evolution by Cancer and Viruses in Evading the NKG2D Immune Response

期刊

CANCERS
卷 12, 期 12, 页码 -

出版社

MDPI
DOI: 10.3390/cancers12123827

关键词

NKG2D ligands; NKG2D receptor; NK cells; immune evasion; convergent evolution; cancer; viruses; immunotherapy

类别

资金

  1. Brain Research UK [STU1617-02]
  2. Cancer Research UK [C552/A29106]

向作者/读者索取更多资源

Simple Summary Cells undergoing stress, viral infection, and malignant transformation express natural killer group 2 member D (NKG2D) ligands on their surface, rendering them susceptible to immunosurveillance. Given this selective pressure exerted on viruses and cancer cells, many viruses and several cancers have evolved means of evading NKG2D recognition. This review highlights the various ways in which stresses, viruses and cancers induce the expression of NKG2D ligands, before comparing the similarities and differences between viral and cancer mechanisms to subsequently prevent recognition by the NKG2D system. The natural killer group 2 member D (NKG2D) receptor and its family of NKG2D ligands (NKG2DLs) are key components in the innate immune system, triggering NK, gamma delta and CD8(+) T cell-mediated immune responses. While surface NKG2DL are rarely found on healthy cells, expression is significantly increased in response to various types of cellular stress, viral infection, and tumour cell transformation. In order to evade immune-mediated cytotoxicity, both pathogenic viruses and cancer cells have evolved various mechanisms of subverting immune defences and preventing NKG2DL expression. Comparisons of the mechanisms employed following virus infection or malignant transformation reveal a pattern of converging evolution at many of the key regulatory steps involved in NKG2DL expression and subsequent immune responses. Exploring ways to target these shared steps in virus- and cancer-mediated immune evasion may provide new mechanistic insights and therapeutic opportunities, for example, using oncolytic virotherapy to re-engage the innate immune system towards cancer cells.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.6
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据