Linked Life Data

15240120

Source:http://linkedlifedata.com/resource/pubmed/id/15240120

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2004-7-8
pubmed:abstractText
Natural killer (NK) cells perform multiple biological functions including tumor cell lysis and eradicating virally infected cells. Here, we report for the first time that D-galactosyl-beta1-1' sphingosine and D-glucosyl-beta1- 1' sphingosine damage human NK cells. We show that these cells express T-cell-associated gene-8, the receptor for glycosphingolipids. D-galactosyl-beta1-1' sphingosine and D-glucosyl-beta1-1' sphingosine induce the in vitro chemotaxis of human NK cells. Both D-galactosyl-beta1-1' sphingosine and D-glucosyl-beta1-1' sphingosine inhibit the cytotoxicity and IFN-gamma secretion by these cells. Further analysis shows that the glycosphingolipids D-galactosyl-beta1-1' sphingosine and D-glucosyl-beta1-1' sphingosine but not any other lipid examined, which include D-lactosyl-beta1-1' sphingosine, sphingosine 1-phosphate, sphingosine, lysophosphatidic acid, and phosphatidic acid, induce the apoptosis, globoid-like formation, and multinucleation in human NK cells. These results may have important implications on diseases where glycosphingolipids accumulate.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0006-291X
pubmed:author
pubmed:issnType
Print
pubmed:day
30
pubmed:volume
320
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
810-5
pubmed:dateRevised
2006-11-20
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
D-galactosyl-beta1-1'-sphingosine and D-glucosyl-beta1-1'-sphingosine induce human natural killer cell apoptosis.
pubmed:affiliation
Department of Anatomy, Institute of Basic Medical Sciences, University of Oslo, P.O.B. 1105 Blindern, N-0317 Oslo, Norway. azzam.maghazachi@basalmed.uio.no
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't