Peptide antagonism as a mechanism for NK cell activation

Lena Fadda; 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

doi:10.1073/pnas.0913745107

Peptide antagonism as a mechanism for NK cell activation

Lena Fadda, 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

Research output: Contribution to journal › Article › peer-review

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.

Original language	English
Pages (from-to)	10160-10165
Number of pages	5
Journal	Proceedings of the National Academy of Sciences of the United States of America
Volume	107
Issue number	22
DOIs	https://doi.org/10.1073/pnas.0913745107
Publication status	Published - 1 Jun 2010

Keywords

Killer cell immunoglobulin-like receptors
MHC class I

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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http://www.pnas.org/content/107/22/10160.full.pdf

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Fadda, L., Borhis, G., Ahmed, P., Cheent, K., Pageon, S. V., Cazaly, A., Stathopoulos, S., Middleton, D., Mulder, A., Claas, F. H. J., Elliott, T., Davis, D. M., Purbhoo, M. A., & Khakoo, S. 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. https://doi.org/10.1073/pnas.0913745107

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title = "Peptide antagonism as a mechanism for NK cell activation",

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.",

keywords = "Killer cell immunoglobulin-like receptors, MHC class I",

author = "Lena Fadda and Gwenoline Borhis and Parvin Ahmed and Kuldeep Cheent and Pageon, {Sophie V.} and Angelica Cazaly and Stavros Stathopoulos and Derek Middleton and Arend Mulder and Claas, {Frans H J} and Tim Elliott and Davis, {Daniel M.} and Purbhoo, {Marco A.} and Khakoo, {Salim I.}",

note = ", Cancer Research UK, United Kingdom, Medical Research Council, United Kingdom, Wellcome Trust, United Kingdom",

year = "2010",

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doi = "10.1073/pnas.0913745107",

language = "English",

volume = "107",

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Fadda, L, Borhis, G, Ahmed, P, Cheent, K, Pageon, SV, Cazaly, A, Stathopoulos, S, Middleton, D, Mulder, A, Claas, FHJ, Elliott, T, Davis, DM, Purbhoo, MA & Khakoo, SI 2010, 'Peptide antagonism as a mechanism for NK cell activation', Proceedings of the National Academy of Sciences of the United States of America, vol. 107, no. 22, pp. 10160-10165. https://doi.org/10.1073/pnas.0913745107

TY - JOUR

T1 - Peptide antagonism as a mechanism for NK cell activation

AU - Fadda, Lena

AU - Borhis, Gwenoline

AU - Ahmed, Parvin

AU - Cheent, Kuldeep

AU - Pageon, Sophie V.

AU - Cazaly, Angelica

AU - Stathopoulos, Stavros

AU - Middleton, Derek

AU - Mulder, Arend

AU - Claas, Frans H J

AU - Elliott, Tim

AU - Davis, Daniel M.

AU - Purbhoo, Marco A.

AU - Khakoo, Salim I.

N1 - , Cancer Research UK, United Kingdom, Medical Research Council, United Kingdom, Wellcome Trust, United Kingdom

PY - 2010/6/1

Y1 - 2010/6/1

N2 - 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.

AB - 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.

KW - Killer cell immunoglobulin-like receptors

KW - MHC class I

U2 - 10.1073/pnas.0913745107

DO - 10.1073/pnas.0913745107

M3 - Article

C2 - 20439706

SN - 0027-8424

VL - 107

SP - 10160

EP - 10165

JO - Proceedings of the National Academy of Sciences of the United States of America

JF - Proceedings of the National Academy of Sciences of the United States of America

IS - 22

ER -

Peptide antagonism as a mechanism for NK cell activation

Abstract

Keywords

UN SDGs

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