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

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.

• Authors: A Müllbacher, M Lobigs
• Journal: Immunity (Immunity) Vol. 3 Issue 2 Pg. 207-14 (Aug 1995) ISSN: 1074-7613 [Print] United States
• PMID: 7544229 (Publication Type: Journal Article)

Chemical References

• ATP Binding Cassette Transporter, Subfamily B, Member 2
• ATP-Binding Cassette Transporters
• Histocompatibility Antigens Class I
• Peptides
• TAP1 protein, human
• Tap1 protein, mouse
• Interferons

Topics

• ATP Binding Cassette Transporter, Subfamily B, Member 2
• ATP-Binding Cassette Transporters (metabolism)
• Animals
• Antigen-Presenting Cells (immunology)
• Cells, Cultured
• Cricetinae
• Endoplasmic Reticulum (metabolism)
• Female
• Flavivirus Infections (immunology)
• Histocompatibility Antigens Class I (metabolism)
• In Vitro Techniques
• Interferons (physiology)
• Mice
• Mice, Inbred BALB C
• Mice, Inbred C3H
• Mice, Inbred C57BL
• Mice, Inbred CBA
• Peptides (immunology, metabolism)
• Up-Regulation