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.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Amino Acid Sequence
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Cell Line
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HLA-C Antigens / metabolism
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Humans
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Killer Cells, Natural / immunology*
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Kinetics
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Ligands
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Lymphocyte Activation
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Oligopeptides / genetics
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Oligopeptides / immunology
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Oligopeptides / metabolism
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Phosphorylation
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Protein Binding
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Proto-Oncogene Proteins c-vav / metabolism
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Receptors, KIR / antagonists & inhibitors
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Receptors, KIR / immunology
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Receptors, KIR2DL2 / antagonists & inhibitors
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Receptors, KIR2DL2 / metabolism
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Receptors, KIR2DL3 / antagonists & inhibitors
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Receptors, KIR2DL3 / metabolism
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Signal Transduction
Substances
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HLA-C Antigens
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KIR2DL2 protein, human
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KIR2DL3 protein, human
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Ligands
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Oligopeptides
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Proto-Oncogene Proteins c-vav
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Receptors, KIR
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Receptors, KIR2DL2
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Receptors, KIR2DL3
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VAV1 protein, human