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Human cytomegalovirus microRNA miR-US4-1 inhibits CD8 + T cell responses by targeting the aminopeptidase ERAP1

Cited 117 time in Web of Science Cited 127 time in Scopus
Authors
Kim, Sungchul; Lee, Sanghyun; Shin, Jinwook; Kim, Youngkyun; Evnouchidou, Irini; Kim, Donghyun; Kim, Young-Kook; Kim, Young-Eui; Ahn, Jin-Hyun; Riddell, Stanley R.; Stratikos, Efstratios; Kim, V. Narry; Ahn, Kwangseog
Issue Date
2011-10
Citation
Nature Immunology, Vol.12 No.10, pp.984-991
Abstract
Major histocompatibility complex (MHC) class I molecules present peptides on the cell surface to CD8(+) T cells, which is critical for the killing of virus-infected or transformed cells. Precursors of MHC class I-presented peptides are trimmed to mature epitopes by the aminopeptidase ERAP1. The US2-US11 genomic region of human cytomegalovirus (HCMV) is dispensable for viral replication and encodes three microRNAs (miRNAs). We show here that HCMV miR-US4-1 specifically downregulated ERAP1 expression during viral infection. Accordingly, the trimming of HCMV-derived peptides was inhibited, which led to less susceptibility of infected cells to HCMV-specific cytotoxic T lymphocytes (CTLs). Our findings identify a previously unknown viral miRNA-based CTL-evasion mechanism that targets a key step in the MHC class I antigen-processing pathway.
ISSN
1529-2908
URI
https://hdl.handle.net/10371/171935
DOI
https://doi.org/10.1038/ni.2097
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College of Natural Sciences (자연과학대학)Dept. of Biological Sciences (생명과학부)Journal Papers (저널논문_생명과학부)
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