Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

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




Journal article


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

Publication Date





10160 - 10165


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


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