Source:http://linkedlifedata.com/resource/pubmed/id/17304104
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
2007-2-16
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pubmed:abstractText |
Hypertonic saline (HS) treatment promotes interleukin (IL)-2 production and enhances T-cell activation by the release of cellular adenosine triphosphate (ATP) that activates P2 nucleotide receptors. Released ATP can be hydrolyzed to adenosine, which inhibits T-cell activation. We examined if adenosine affects the response of T cells to HS treatment, and found that the amount of ATP released from T cells is a function of the HS concentration and duration of HS exposure. Physiologically relevant HS concentrations (<40 mmol/L) induced rapid ATP release, with the highest ATP concentrations released within 1 min. The released ATP was converted to adenosine, which opposed the enhancing effects of HS on IL-2 production. We found that Jurkat and CD4+ primary human T cells express most abundantly the A2A and A2B adenosine receptor subtypes, which mediate the suppressive effects of adenosine, as the A2 receptor agonist CGS 21680 suppressed IL-2 production, whereas the A2 receptor antagonist 3,7-dimethyl-1-(2-propynyl)xanthine augmented the enhancing effect of HS on T-cell function. Elimination of extracellular adenosine by adding exogenous adenosine deaminase also increased the enhancing effects of HS. These data suggest that the effect of HS treatment on T-cell function can be modulated with pharmacological agents that abolish the suppressive effects of adenosine formed from the ATP that is released in response to HS treatment.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Adenosine,
http://linkedlifedata.com/resource/pubmed/chemical/Adenosine Deaminase,
http://linkedlifedata.com/resource/pubmed/chemical/Adenosine Triphosphate,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-2,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Purinergic P1,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium Chloride
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
1073-2322
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
27
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
242-50
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:17304104-Adenosine,
pubmed-meshheading:17304104-Adenosine Deaminase,
pubmed-meshheading:17304104-Adenosine Triphosphate,
pubmed-meshheading:17304104-Cell Separation,
pubmed-meshheading:17304104-Humans,
pubmed-meshheading:17304104-Hydrolysis,
pubmed-meshheading:17304104-Interleukin-2,
pubmed-meshheading:17304104-Jurkat Cells,
pubmed-meshheading:17304104-Leukocytes, Mononuclear,
pubmed-meshheading:17304104-Models, Biological,
pubmed-meshheading:17304104-Receptors, Purinergic P1,
pubmed-meshheading:17304104-Sodium Chloride,
pubmed-meshheading:17304104-Stress, Physiological,
pubmed-meshheading:17304104-T-Lymphocytes,
pubmed-meshheading:17304104-Time Factors
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pubmed:year |
2007
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pubmed:articleTitle |
Hypertonic stress regulates T-cell function by the opposing actions of extracellular adenosine triphosphate and adenosine.
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pubmed:affiliation |
Surgical Immunology Research Laboratory, Department of Surgery, Division of Trauma, University of California San Diego, San Diego, California 92103-8236, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, N.I.H., Extramural
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