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• W2028267776 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." @default.
• W2028267776 created "2016-06-24" @default.
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• W2028267776 date "2011-09-04" @default.
• W2028267776 modified "2023-10-14" @default.
• W2028267776 title "Human cytomegalovirus microRNA miR-US4-1 inhibits CD8+ T cell responses by targeting the aminopeptidase ERAP1" @default.
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• W2028267776 doi "https://doi.org/10.1038/ni.2097" @default.
• W2028267776 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3526977" @default.
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