HLA-E binds to natural killer cell receptors CD94/NKG2A, B and C

Veronique M. Braud (), David S. J. Allan, Christopher A. O'Callaghan, Kalle Söderström, Annalisa D'Andrea, Graham S. Ogg, Sasha Lazetic, Neil T. Young, John I. Bell, Joseph H. Phillips, Lewis L. Lanier and Andrew J. McMichael
Additional contact information
Veronique M. Braud: Institute of Molecular Medicine, John Radcliffe Hospital
David S. J. Allan: Institute of Molecular Medicine, John Radcliffe Hospital
Christopher A. O'Callaghan: Institute of Molecular Medicine, John Radcliffe Hospital
Kalle Söderström: DNAX Research Institute of Molecular and Cellular Biology
Annalisa D'Andrea: DNAX Research Institute of Molecular and Cellular Biology
Graham S. Ogg: Institute of Molecular Medicine, John Radcliffe Hospital
Sasha Lazetic: DNAX Research Institute of Molecular and Cellular Biology
Neil T. Young: John Radcliffe Hospital
John I. Bell: Institute of Molecular Medicine, John Radcliffe Hospital
Joseph H. Phillips: DNAX Research Institute of Molecular and Cellular Biology
Lewis L. Lanier: DNAX Research Institute of Molecular and Cellular Biology
Andrew J. McMichael: Institute of Molecular Medicine, John Radcliffe Hospital

Nature, 1998, vol. 391, issue 6669, 795-799

Abstract: Abstract The protein HLA-E is a non-classical major histocompatibility complex (MHC) molecule of limited sequence variability. Its expression on the cell surface is regulated by the binding of peptides derived from the signal sequence of some other MHC class I molecules1,2. Here we report the identification of ligands for HLA-E. We constructed tetramers3 in which recombinant HLA-E and β2-microglobulin were refolded with an MHC leader-sequence peptide, biotinylated, and conjugated to phycoerythrin-labelled Extravidin. This HLA-E tetramer bound to natural killer (NK) cells and a small subset of T cells from peripheral blood. On transfectants, the tetramer bound to the CD94/NKG2A, CD94/NKGK2B and CD94/NKG2C NK cell receptors, but did not bind to the immunoglobulin family of NK cell receptors (KIR). Surface expression of HLA-E was enough to protect target cells from lysis by CD94/NKG2A+ NK-cell clones. A subset of HLA class I alleles has been shown to inhibit killing by CD94/NKG2A+ NK-cell clones4,5,6. Only the HLA alleles that possess a leader peptide capable of upregulating HLA-E surface expression confer resistance to NK-cell-mediated lysis, implying that their action is mediated by HLA-E, the predominant ligand for the NK cell inhibitory receptor CD94/NKG2A.

Date: 1998
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DOI: 10.1038/35869

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