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
  • 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.