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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.

Author information

1
Division of Cell Biology, John Curtin School of Medical Research, Australian National University, Canberra.

Abstract

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.

PMID:
7544229
DOI:
10.1016/1074-7613(95)90090-x
[Indexed for MEDLINE]
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