Abstract
US11 and US2 encode gene products expressed early in the replicative cycle of human cytomegalovirus (HCMV), which cause dislocation of human and murine major histocompatibility complex (MHC) class I molecules from the lumen of the endoplasmic reticulum to the cytosol, where the class I heavy chains are rapidly degraded. Human histocompatibility leukocyte antigens (HLA)-C and HLA-G are uniquely resistant to the effects of both US11 and US2 in a human trophoblast cell line as well as in porcine endothelial cells stably transfected with human class I genes. Dislocation and degradation of MHC class I heavy chains do not appear to involve cell type-specific factors, as US11 and US2 are fully active in this xenogeneic model. Importantly, trophoblasts HLA-G and HLA-C possess unique characteristics that allow their escape from HCMV-associated MHC class I degradation. Trophoblast class I molecules could serve not only to block recognition by natural killer cells, but also to guide virus-specific HLA-C-and possibly HLA-G-restricted cytotoxic T-lymphocytes to their targets.
Original language | English |
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Pages (from-to) | 497-503 |
Number of pages | 7 |
Journal | Journal of Experimental Medicine |
Volume | 188 |
Issue number | 3 |
DOIs | |
State | Published - 3 Aug 1998 |
Externally published | Yes |
Keywords
- Cytomegalovirus
- HLA-G
- Human
- MHC class I
- Trophoblast