Peptide antagonism as a mechanism for NK cell activation

Author(s):
Fadda, L.; Borhis, G.; Ahmed, P.; Cheent, K.; Pageon, S.V.; Cazaly, A.; Stathopoulos, S.; Middleton, D.; Mulder, A.; Claas, F.H.J. (0000-0003-4157-6201); Elliott, T.; Davis, D.M.; Purbhoo, M.A.; Khakoo, S.I.
Published
2010
Publication type
Article / Letter to editor

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.

killer cell immunoglobulin-like receptors MHC class I mhc class-i inhibitory receptor genes immunoglobulin-like receptor c virus-infection complex class-i hla class-i mediated lysis direct binding cutting edge recognition
Date issued
2010-06-01
Language
English
Is part of
Proceedings of the National Academy of Sciences (2010), Vol. 107, no. 22, p. 10160-10165
hdl
1887/108775
doi
10.1073/pnas.0913745107