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J. Exp. Med.,
Volume 188, Number 3, August 3, 1998 497-503
By

From the * Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115; and the 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.
Transplantation Biology Research Center, Massachusetts General Hospital, Boston,
Massachusetts 02119
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