Peptide antagonism as a mechanism for NK cell activation

Proc Natl Acad Sci U S A. 2010 Jun 1;107(22):10160-5. doi: 10.1073/pnas.0913745107.

Lena Fadda ¹, Gwenoline Borhis, Parvin Ahmed, Kuldeep Cheent, Sophie V Pageon, Angelica Cazaly, Stavros Stathopoulos, Derek Middleton, Arend Mulder, Frans H J Claas, Tim Elliott, Daniel M Davis, Marco A Purbhoo, Salim I Khakoo

Affiliations

Affiliation

1 Divisions of Medicine and Cell and Molecular Medicine, Imperial College London, London W2 1PG, United Kingdom.

PMID: 20439706 DOI: 10.1073/pnas.0913745107

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.

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