Peptide antagonism as a mechanism for NK cell activation
L Fadda, G Borhis, P Ahmed… - Proceedings of the …, 2010 - National Acad Sciences
L Fadda, G Borhis, P Ahmed, K Cheent, SV Pageon, A Cazaly, S Stathopoulos, D Middleton…
Proceedings of the National Academy of Sciences, 2010•National Acad SciencesInhibition 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.
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.
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.
National Acad Sciences
