Peptide antagonism as a mechanism for NK Cell activation


Fadda, Lena, Borhis, Gwenoline, Ahmed, Parvin, Cheent, Kuldeep, Pageon, Sophie V., Cazaly, Angelica, Stathopoulos, Stavros, Middleton, Derek, Mulder, Arend, Claas, Frans H.J., Elliott, Tim, Davis, Daniel M., Purbhoo, Marco A. and Khakoo, Salim I. (2010) Peptide antagonism as a mechanism for NK Cell activation Proceedings of the National Academy of Sciences of the United States of America, 107, (22), pp. 10160-10165. (doi:10.1073/pnas.0913745107). (PMID:20534579).

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Description/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.

Item Type: Article
Digital Object Identifier (DOI): doi:10.1073/pnas.0913745107
ISSNs: 0027-8424 (print)
Keywords: killer cell immunoglobulin-like receptors, mhc class I
Subjects: Q Science > QR Microbiology > QR180 Immunology
R Medicine > RC Internal medicine > RC0254 Neoplasms. Tumors. Oncology (including Cancer)
ePrint ID: 148951
Date :
Date Event
1 June 2010Published
Date Deposited: 04 May 2010 15:49
Last Modified: 21 Feb 2017 02:19
Further Information:Google Scholar
URI: http://eprints.soton.ac.uk/id/eprint/148951

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