Linked Life Data

11397476

Source:http://linkedlifedata.com/resource/pubmed/id/11397476

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2001-6-8
pubmed:abstractText
Persistent lymphocytosis in large granular lymphocyte leukemia (LGL) may result from defects in activation- or Fas crosslinking-induced cell death. Here we show that Fas crosslinking and CD3 activation causes apoptosis of in vitro activated CD8 T cells, but not of freshly isolated CD8 T cells. Death was partially blocked by a neutralizing antibody to FasL. Inhibition of metalloproteinase-mediated FasL solubilization significantly potentiated induction of cell death. Furthermore, CD3 plus CD28 stimulation resulted in telomeric erosion in LGL cells, and ultimately proliferation ceased. Together, these data indicate that activation- and proliferation-related cell death mechanisms are functional in LGL cells.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0145-2126
pubmed:author
pubmed:issnType
Print
pubmed:volume
25
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
699-708
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
CD8+ T cells in large granular lymphocyte leukemia are not defective in activation- and replication-related apoptosis.
pubmed:affiliation
Bone Marrow Transplant Unit, Hematology Branch, NHLBI, National Institutes of Health, Building 10, Room 7c103, 9000 Rockville Pike, Bethesda, MD 20892, USA. melenhoj@nih.gov
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.