Linked Life Data

9010264

Source:http://linkedlifedata.com/resource/pubmed/id/9010264

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1997-2-21
pubmed:abstractText
The in vitro treatment of lpr thymocytes with FTY720 resulted in a dose-dependent reduction in cell viability due to apoptosis. In order to study the effect of FTY720 in vivo, lpr mice received an oral daily dose of 1 mg/kg FTY720 for 14 days, beginning at 16 weeks of age which was when the animals were developing massive lymphoadenopathy. Compared with untreated lpr mice, FTY720-treated lpr mice had significantly prolonged lives. At 24 weeks of age, treated mice demonstrated markedly reduced weights of the spleen and lymph nodes, and the proportion of CD3+ B220+ and CD4- CD8- cells in the thymus, spleen and lymph nodes decreased markedly. In addition, in these mice the percentage of CD4+ CD8+ and CD3- B220- cells in the thymus and the percentage of CD4+ CD8-, CD4- CD8+, CD3+ B220- and CD3- B220+ cells in the spleen returned to almost the normal values observed in wild-type mice. Histological observation 1 day after the final administration of FTY720 revealed a remarkable infiltration of neutrophils in the lymphoid organs. Apoptotic cells were detected in all the lymphoid organs using in situ DNA nick-end labelling. Electron microscopy showed that the apoptotic cells were ingested by phagocytes. FTY720 therapy is thus highly effective in Fas-mutant animals with abnormally expanding lymphocytes.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0009-9104
pubmed:author
pubmed:issnType
Print
pubmed:volume
107
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
103-11
pubmed:dateRevised
2008-11-20
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
The in vivo induction of lymphocyte apoptosis in MRL-lpr/lpr mice treated with FTY720.
pubmed:affiliation
Department of Experimental Surgery and Bioengineering, National Children's Medical Research Center, Tokyo, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't