Linked Life Data

11145664

Source:http://linkedlifedata.com/resource/pubmed/id/11145664

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2001-1-26
pubmed:abstractText
NK cell function is regulated by cytokines and certain biochemical mediators in a positive or negative manner. This study was performed to investigate the suppressive effects of PGE(2) on IL-15-activated human NK cell function. Purified NK cells were cultured with 200 ng/ml IL-15 for 2 days in the presence or absence of 10-200 ng/ml PGE(2). PGE(2) significantly suppressed NK cell-mediated cytotoxicity and IFN-gamma production at the secretional and the transcriptional levels. We also evaluated the effect of PGE(2) on the IL-15R complex that consists of IL-2Rbeta, common gamma-chain (gamma(c)-chain), and a specific chain IL-15Ralpha. Percentage of positive cells and number of binding sites for gamma(c)-chain were significantly increased after IL-15 treatment; however, a substantial decrease was observed with PGE(2) cotreatment. In contrast, constitutive expression of IL-2Rbeta was significantly decreased after IL-15 treatment, with no change detected in the presence of PGE(2.) At the transcriptional level, neither IL-15 nor PGE(2) had significant effects on the expression of beta- or gamma(c)-chains. There was a 3-fold increase in the expression of IL-15Ralpha at the transcriptional level that peaked at 8 h after IL-15 treatment; however, PGE(2) had no significant effect. Suppression of NK function by PGE(2) was not due to the endogenous production of IL-4, IL-10, or TGF-beta(1) by NK cells. These results suggest that down-regulation of surface expression of gamma(c)-chain on NK cells may be one mechanism through which PGE(2) mediates suppression of IL-15-activated NK cell function.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Dinoprostone, http://linkedlifedata.com/resource/pubmed/chemical/IL15RA protein, human, http://linkedlifedata.com/resource/pubmed/chemical/IL2RG protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Immunosuppressive Agents, http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma, http://linkedlifedata.com/resource/pubmed/chemical/Interleukin Receptor Common gamma..., http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-15, http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-15, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-2, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-7
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
166
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
885-91
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
Prostaglandin E2 suppressed IL-15-mediated human NK cell function through down-regulation of common gamma-chain.
pubmed:affiliation
Departments of. Surgery and Microbiology, University of Mississippi Medical Center, Jackson, MS 39216, USA. pjoshi@surgery.umsmed.edu
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't