Reduced cell surface expression of HLA-C molecules correlates with restricted peptide binding and stable TAP interaction

J Immunol. 1998 Jan 1;160(1):171-9.

Abstract

HLA-C molecules are poorly expressed at the cell surface compared with HLA-A and HLA-B locus products. The reason for the low surface expression and the underlying mechanism is unclear. We show that the HLA-C4 allele is expressed intracellularly in amounts similar to HLA-A and HLA-B alleles. However, the majority of the HLA-C4 molecules is not transported, but is retained in the endoplasmic reticulum by stable interaction with TAP. This pool does not appear to participate in the formation of HLA-C4/peptide complexes, but is degraded in the endoplasmic reticulum. HLA-C4 molecules can dissociate from TAP upon binding of specific peptide. However, they require a 10-fold higher concentration of a completely degenerated 9-mer peptide mixture for release from TAP than the HLA-A and HLA-B alleles. Our data show that the HLA-C molecules tested are more selective in their peptide binding than HLA-A and HLA-B molecules, resulting in prolonged association with TAP and a reduced formation of intracellular HLA-C/peptide complexes. The restricted peptide binding of certain HLA-C alleles provides one explanation for the reduced expression of HLA-C molecules at the cell surface. Other mechanisms will be discussed.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • ATP Binding Cassette Transporter, Subfamily B, Member 2
  • ATP-Binding Cassette Transporters / metabolism*
  • Alleles
  • B-Lymphocytes / metabolism*
  • B-Lymphocytes / ultrastructure
  • Binding, Competitive
  • Cell Membrane / metabolism
  • Cells, Cultured
  • Endoplasmic Reticulum / metabolism
  • HLA-C Antigens / metabolism*
  • Humans
  • Intracellular Membranes / metabolism
  • Peptides / metabolism
  • Protein Binding

Substances

  • ATP Binding Cassette Transporter, Subfamily B, Member 2
  • ATP-Binding Cassette Transporters
  • HLA-C Antigens
  • Peptides
  • TAP1 protein, human