A Peptideantagonist disrupts NK cell inhibitory synapse formation
A Peptideantagonist disrupts NK cell inhibitory synapse formation
Productive engagement of MHC class I by inhibitory NK cell receptors depends on the peptide bound by the MHC class I molecule. Peptide:MHC complexes that bind weakly to killer cell Ig-like receptors (KIRs) can antagonize the inhibition mediated by high-affinity peptide:MHC complexes and cause NK cell activation. We show that low-affinity peptide:MHC complexes stall inhibitory signaling at the step of Src homology protein tyrosine phosphatase 1 recruitment and do not go on to form the KIR microclusters induced by high-affinity peptide:MHC, which are associated with Vav dephosphorylation and downstream signaling. Furthermore, the low-affinity peptide:MHC complexes prevented the formation of KIR microclusters by high-affinity peptide:MHC. Thus, peptide antagonism of NK cells is an active phenomenon of inhibitory synapse disruption.
2924-2930
Borhis, G.
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Ahmed, P.S.
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Mbiribindi, B.
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Naiyer, M.M.
b4ac5546-4f7d-462c-9632-a60a552ea3b3
Davis, D.M.
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Purbhoo, M.A.
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Khakoo, S.I.
6c16d2f5-ae80-4d9b-9100-6bfb34ad0273
2013
Borhis, G.
36af18f7-e0eb-4f5f-9df4-2801299f1dcd
Ahmed, P.S.
dd3b8c28-5954-4df3-964b-d76ca4c93d68
Mbiribindi, B.
6a6d23a6-b91b-408a-a910-8a5d5ba0386d
Naiyer, M.M.
b4ac5546-4f7d-462c-9632-a60a552ea3b3
Davis, D.M.
b14d3fae-303d-491c-b011-dc096b0e859e
Purbhoo, M.A.
3f11373c-6ea6-4860-87ec-acaed71963ac
Khakoo, S.I.
6c16d2f5-ae80-4d9b-9100-6bfb34ad0273
Borhis, G., Ahmed, P.S., Mbiribindi, B., Naiyer, M.M., Davis, D.M., Purbhoo, M.A. and Khakoo, S.I.
(2013)
A Peptideantagonist disrupts NK cell inhibitory synapse formation.
Journal of Immunology, 190 (6), .
(doi:10.4049/jimmunol.1201032).
(PMID:23382564)
Abstract
Productive engagement of MHC class I by inhibitory NK cell receptors depends on the peptide bound by the MHC class I molecule. Peptide:MHC complexes that bind weakly to killer cell Ig-like receptors (KIRs) can antagonize the inhibition mediated by high-affinity peptide:MHC complexes and cause NK cell activation. We show that low-affinity peptide:MHC complexes stall inhibitory signaling at the step of Src homology protein tyrosine phosphatase 1 recruitment and do not go on to form the KIR microclusters induced by high-affinity peptide:MHC, which are associated with Vav dephosphorylation and downstream signaling. Furthermore, the low-affinity peptide:MHC complexes prevented the formation of KIR microclusters by high-affinity peptide:MHC. Thus, peptide antagonism of NK cells is an active phenomenon of inhibitory synapse disruption.
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Published date: 2013
Organisations:
Clinical & Experimental Sciences
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Local EPrints ID: 356241
URI: http://eprints.soton.ac.uk/id/eprint/356241
ISSN: 0022-1767
PURE UUID: a2de4cac-50db-4a23-86ea-c6c511ea9e00
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Date deposited: 17 Sep 2013 11:01
Last modified: 15 Mar 2024 03:12
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Author:
G. Borhis
Author:
P.S. Ahmed
Author:
B. Mbiribindi
Author:
M.M. Naiyer
Author:
D.M. Davis
Author:
M.A. Purbhoo
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