Peptide antagonism as a mechanism for NK cell activation
Fadda L., Borhis G., Ahmed P., Cheent K., Pageon SV., Cazaly A., Stathopoulos S., Middleton D., Mulder A., Claas FHJ., Elliott T., Davis DM., Purbhoo MA., Khakoo SI.
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.