生物
主要组织相容性复合体
MHC I级
抗原呈递
抗原处理
免疫系统
癌症研究
免疫学
MHC限制
自然杀伤细胞
细胞毒性T细胞
细胞
病毒学
T细胞
遗传学
体外
作者
Graham Bottley,Watherston Og,Hiew Yl,Bodil Norrild,Graham P. Cook,G. Eric Blair
出处
期刊:Oncogene
[Springer Nature]
日期:2007-09-10
卷期号:27 (12): 1794-1799
被引量:56
标识
DOI:10.1038/sj.onc.1210798
摘要
High-risk human papillomavirus (HPV) is a major causative agent of cervical cancer and the E6 and E7 genes encode the major HPV oncoproteins. The E7 protein from high-risk HPV types alters cell cycle progression and represses genes encoding components of the antigen-presentation pathway, suggesting a role for E7 in tumour immune evasion. We show that knockdown of E7 expression in HPV16- and HPV18-transformed cervical carcinoma cells by RNA interference increased expression of major histocompatibility complex (MHC) class I at the cell surface and reduced susceptibility of these cells to natural killer (NK) cells. Tetracycline-regulated induction of HPV16 E7 resulted in reduced expression of cell surface MHC class I molecules and increased NK cell killing. Our results suggest that, for HPV-associated malignancies, reduced MHC class I expression is the result of an active immune evasion strategy that has evolved to assist viral replication.
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