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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), 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
ISSN:0027-8424 (print)
1091-6490 (electronic)
Uncontrolled Keywords:killer cell immunoglobulin-like receptors, mhc class I
Related URLs:
Subjects:Q Science > QR Microbiology > QR180 Immunology
R Medicine > RC Internal medicine > RC0254 Neoplasms. Tumors. Oncology (including Cancer)
Divisions:University Structure - Pre August 2011 > School of Medicine > Cancer Sciences
ePrint ID:148951
Deposited On:04 May 2010 16:49
Last Modified:01 Jun 2011 04:22

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