Peptide antagonism as a mechanism for NK cell activation
2010
Fadda, Lena | Borhis, Gwenoline | Ahmed, Parvin | Cheent, Kuldeep | Pageon, Sophie V. | Cazaly, Angelica | Stathopoulos, Stavros | Middleton, Derek | Mulder, Arend | Claas, Frans H.J. | Elliott, T. J. (Tim J) | Davis, Daniel M. | Purbhoo, Marco A. | Khakoo, Salim I.
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.
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