Dissemin is shutting down on January 1st, 2025

Published in

National Academy of Sciences, Proceedings of the National Academy of Sciences, 22(107), p. 10160-10165, 2010

DOI: 10.1073/pnas.0913745107

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Peptide antagonism as a mechanism for NK cell activation

This paper is made freely available by the publisher.
This paper is made freely available by the publisher.

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Abstract

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.