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Inhibition of natural killer (NK) cells is mediated by MHC class I receptors including the killer cell Ig-like receptor (KIR). We demonstrate that HLA-C binding peptides can function as altered peptide ligands for KIR and antagonize the inhibition mediated by KIR2DL2/KIR2DL3. Antagonistic peptides promote clustering of KIR at the interface of effector and target cells, but do not result in inhibition of NK cells. Our data show that, as for T cells, small changes in the peptide content of MHC class I can regulate NK cell activity.

Original publication

DOI

10.1073/pnas.0913745107

Type

Journal article

Journal

Proceedings of the National Academy of Sciences of the United States of America

Publication Date

06/2010

Volume

107

Pages

10160 - 10165

Addresses

Divisions of Medicine and Cell and Molecular Medicine, Imperial College London, London W2 1PG, United Kingdom.

Keywords

Killer Cells, Natural, Cell Line, Humans, Oligopeptides, HLA-C Antigens, Ligands, Lymphocyte Activation, Signal Transduction, Amino Acid Sequence, Protein Binding, Phosphorylation, Kinetics, Proto-Oncogene Proteins c-vav, Receptors, KIR, Receptors, KIR2DL2, Receptors, KIR2DL3