Switch to
| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
9
|
| pubmed:dateCreated |
1998-12-2
|
| pubmed:abstractText |
Immunologically privileged sites have been shown to express Fas ligand (FasL) and may protect themselves by inducing apoptosis of infiltrating inflammatory cells. We asked whether the Fas/FasL interaction could be used to protect a xenograft from rejection. We proposed that endothelial cells that are resistant to Fas-mediated killing could be considered as a vehicle for expression of recombinant FasL.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Nov
|
| pubmed:issn |
0041-1337
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:day |
15
|
| pubmed:volume |
66
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
1126-31
|
| pubmed:dateRevised |
2006-11-15
|
| pubmed:meshHeading |
pubmed-meshheading:9825805-Animals,
pubmed-meshheading:9825805-Aorta,
pubmed-meshheading:9825805-Apoptosis,
pubmed-meshheading:9825805-Cattle,
pubmed-meshheading:9825805-Cell Death,
pubmed-meshheading:9825805-Endothelium, Vascular,
pubmed-meshheading:9825805-Fas Ligand Protein,
pubmed-meshheading:9825805-Graft Rejection,
pubmed-meshheading:9825805-Humans,
pubmed-meshheading:9825805-Jurkat Cells,
pubmed-meshheading:9825805-Leukocytes, Mononuclear,
pubmed-meshheading:9825805-Membrane Glycoproteins,
pubmed-meshheading:9825805-Models, Immunological
|
| pubmed:year |
1998
|
| pubmed:articleTitle |
Regulated and endothelial cell-specific expression of Fas ligand: an in vitro model for a strategy aiming at inhibiting xenograft rejection.
|
| pubmed:affiliation |
Sandoz Center for Immunobiology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA. hien.tran@rzmail.uni-erlangen.de
|
| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|