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ATP secreted by endothelial cells blocks CX3CL1-elicited natural killer cell chemotaxis and cytotoxicity via P2Y11 receptor activation

Endothelial cells (ECs) represent a major source of actively secreted adenosine triphosphate (ATP). Natural killer (NK) cells can mediate vascular injury in several pathologic conditions, including cytomegalovirus infection and vascular leak syndrome. We studied NK-cell expression of P2 receptors an... Full description

Journal Title: Blood 11/25/2010, Vol.116(22), pp.4492-4500
Main Author: Gorini, S.
Other Authors: Callegari, G. , Romagnoli, G. , Mammi, C. , Mavilio, D. , Rosano, G. , Fini, M. , Di Virgilio, F. , Gulinelli, S. , Falzoni, S. , Cavani, A. , Ferrari, D. , La Sala, A.
Format: Electronic Article Electronic Article
Language: English
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ID: ISSN: 0006-4971 ; E-ISSN: 1528-0020 ; DOI: http://dx.doi.org/10.1182/blood-2009-12-260828
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recordid: crossref10.1182/blood-2009-12-260828
title: ATP secreted by endothelial cells blocks CX3CL1-elicited natural killer cell chemotaxis and cytotoxicity via P2Y11 receptor activation
format: Article
creator:
  • Gorini, S.
  • Callegari, G.
  • Romagnoli, G.
  • Mammi, C.
  • Mavilio, D.
  • Rosano, G.
  • Fini, M.
  • Di Virgilio, F.
  • Gulinelli, S.
  • Falzoni, S.
  • Cavani, A.
  • Ferrari, D.
  • La Sala, A.
subjects:
  • Medicine
  • Biology
  • Chemistry
  • Anatomy & Physiology
ispartof: Blood, 11/25/2010, Vol.116(22), pp.4492-4500
description: Endothelial cells (ECs) represent a major source of actively secreted adenosine triphosphate (ATP). Natural killer (NK) cells can mediate vascular injury in several pathologic conditions, including cytomegalovirus infection and vascular leak syndrome. We studied NK-cell expression of P2 receptors and the role of these nucleotide receptors in the regulation of endothelial-NK cell cross-talk. NK cells from healthy subjects expressed P2Y(₁,₂,₄,₆,₁₁,₁₂,₁₃,₁₄) and P2X(₁,₄,₅,₆,₇) receptors. NK cells stimulated with ATP, but not uridine triphosphate, increased intracellular Ca²(+) and chemokinesis. Moreover, ATP, but not uridine triphosphate, inhibited NK chemotaxis in response to CX₃CL1, whereas chemotaxis to CXCL12 was increased. CX₃CL1 elicited killing of human umbilical vein ECs and human coronary artery ECs by NK cells. However, in the presence of ATP, CX₃CL1 failed to stimulate killing of ECs. Such inhibitory effect was lost on exogenous addition of the ATP-hydrolyzing enzyme apyrase or by pharmacologic inhibition of the P2Y₁₁R, and correlated with increased intracellular cyclic adenosine monophosphate concentrations induced by ATP or other P2Y₁₁R agonists, including NAD(+). Extracellular ATP regulates NK-cell cytotoxicity via P2Y₁₁R activation, protecting ECs from CX₃CL1-elicited NK cell-mediated killing. These findings point out the P2Y₁₁R as a potential target for pharmacologic intervention aimed at reducing NK-mediated vascular injury.
language: eng
source:
identifier: ISSN: 0006-4971 ; E-ISSN: 1528-0020 ; DOI: http://dx.doi.org/10.1182/blood-2009-12-260828
fulltext: fulltext
issn:
  • 00064971
  • 0006-4971
  • 15280020
  • 1528-0020
url: Link


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titleATP secreted by endothelial cells blocks CX3CL1-elicited natural killer cell chemotaxis and cytotoxicity via P2Y11 receptor activation
creatorGorini, S. ; Callegari, G. ; Romagnoli, G. ; Mammi, C. ; Mavilio, D. ; Rosano, G. ; Fini, M. ; Di Virgilio, F. ; Gulinelli, S. ; Falzoni, S. ; Cavani, A. ; Ferrari, D. ; La Sala, A.
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descriptionEndothelial cells (ECs) represent a major source of actively secreted adenosine triphosphate (ATP). Natural killer (NK) cells can mediate vascular injury in several pathologic conditions, including cytomegalovirus infection and vascular leak syndrome. We studied NK-cell expression of P2 receptors and the role of these nucleotide receptors in the regulation of endothelial-NK cell cross-talk. NK cells from healthy subjects expressed P2Y(₁,₂,₄,₆,₁₁,₁₂,₁₃,₁₄) and P2X(₁,₄,₅,₆,₇) receptors. NK cells stimulated with ATP, but not uridine triphosphate, increased intracellular Ca²(+) and chemokinesis. Moreover, ATP, but not uridine triphosphate, inhibited NK chemotaxis in response to CX₃CL1, whereas chemotaxis to CXCL12 was increased. CX₃CL1 elicited killing of human umbilical vein ECs and human coronary artery ECs by NK cells. However, in the presence of ATP, CX₃CL1 failed to stimulate killing of ECs. Such inhibitory effect was lost on exogenous addition of the ATP-hydrolyzing enzyme apyrase or by pharmacologic inhibition of the P2Y₁₁R, and correlated with increased intracellular cyclic adenosine monophosphate concentrations induced by ATP or other P2Y₁₁R agonists, including NAD(+). Extracellular ATP regulates NK-cell cytotoxicity via P2Y₁₁R activation, protecting ECs from CX₃CL1-elicited NK cell-mediated killing. These findings point out the P2Y₁₁R as a potential target for pharmacologic intervention aimed at reducing NK-mediated vascular injury.
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date2010-11-25