Peptide antagonism as a mechanism for NK Cell activation
Peptide antagonism as a mechanism for NK Cell activation
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
10160-10165
Fadda, Lena
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Borhis, Gwenoline
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Ahmed, Parvin
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Cheent, Kuldeep
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Pageon, Sophie V.
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Cazaly, Angelica
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Stathopoulos, Stavros
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Middleton, Derek
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Mulder, Arend
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Claas, Frans H.J.
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Elliott, Tim
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Davis, Daniel M.
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Purbhoo, Marco A.
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Khakoo, Salim I.
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1 June 2010
Fadda, Lena
aa39ca15-e356-4617-a1b9-4fa7d91e2bec
Borhis, Gwenoline
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Ahmed, Parvin
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Cheent, Kuldeep
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Pageon, Sophie V.
bd5a2b84-4f7a-43a4-b07d-e176759cfb84
Cazaly, Angelica
944b91cc-ab19-463c-ad08-a6b04c6e628d
Stathopoulos, Stavros
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Middleton, Derek
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Mulder, Arend
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Claas, Frans H.J.
11a3dc77-f915-4086-b7f4-b8632f998cb3
Elliott, Tim
16670fa8-c2f9-477a-91df-7c9e5b453e0e
Davis, Daniel M.
fe125d3a-075a-44b0-9e8b-d84c6c2e2035
Purbhoo, Marco A.
990498b1-eb64-406b-875a-181e9ffd94df
Khakoo, Salim I.
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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), .
(doi:10.1073/pnas.0913745107).
(PMID:20534579)
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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Published date: 1 June 2010
Keywords:
killer cell immunoglobulin-like receptors, mhc class I
Organisations:
Cancer Sciences
Identifiers
Local EPrints ID: 148951
URI: http://eprints.soton.ac.uk/id/eprint/148951
ISSN: 0027-8424
PURE UUID: d8b22320-0f25-4a55-b254-21d6ff6f5e2e
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Date deposited: 04 May 2010 15:49
Last modified: 14 Mar 2024 02:46
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Contributors
Author:
Lena Fadda
Author:
Gwenoline Borhis
Author:
Parvin Ahmed
Author:
Kuldeep Cheent
Author:
Sophie V. Pageon
Author:
Angelica Cazaly
Author:
Stavros Stathopoulos
Author:
Derek Middleton
Author:
Arend Mulder
Author:
Frans H.J. Claas
Author:
Daniel M. Davis
Author:
Marco A. Purbhoo
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