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Immunity. 1995 Aug;3(2):207-14.

Up-regulation of MHC class I by flavivirus-induced peptide translocation into the endoplasmic reticulum.

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Division of Cell Biology, John Curtin School of Medical Research, Australian National University, Canberra.


Flavivirus infection of mammalian cells increases the cell surface expression of major histocompatibility complex (MHC) class I molecules, the recognition elements for cytotoxic T cells. Here, we show that the mechanism for flavivirus-induced up-regulation of class I MHC involves an increase in peptide supply to the endoplasmic reticulum. Flavivirus-mediated peptide supply for MHC class I assembly is independent of the peptide transporters for class I antigen presentation, since infection of class I MHC peptide transport-deficient cell lines with flaviviruses results in the cell surface expression of biologically functional class I MHC peptide complexes. The flavivirus-induced supply of antigenic peptides to the endoplasmic reticulum is not restricted to flavivirus-encoded peptides and independent of interferon. The data imply that peptide availability regulates surface expression of class I MHC restriction elements and suggests a mechanism for flavivirus-induced immunopathology.

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