Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2001-10-9
pubmed:abstractText
NK cells mediate acute rejection of MHC class I-deficient bone marrow cell (BMC) grafts. However, the exact cytotoxic mechanisms of NK cells during acute BMC graft rejection are not well defined. Although the granule exocytosis pathway plays a major role in NK cell-mediated rejection, alternative perforin-independent mechanisms also exist. By analyzing the anti-apoptotic effects of cellular Fas-associated death domain-like IL-1-converting enzyme-inhibitory protein (cFLIP) overexpression, we investigated the possible role of death receptor-induced apoptosis in NK cell-mediated cytotoxicity. In the absence of perforin, we found that cFLIP overexpression reduces lysis of tumor cells by NK cells in vitro and in vivo. In addition, perforin-deficient NK cells were impaired in their ability to acutely reject cFLIP-overexpressing TAP-1 knockout stem cells. These results emphasize the importance of NK cell death receptor-mediated killing during BMC grafts in the absence of perforin.
pubmed:grant
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
167
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
4230-7
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:11591744-Animals, pubmed-meshheading:11591744-Apoptosis, pubmed-meshheading:11591744-Bone Marrow Transplantation, pubmed-meshheading:11591744-CASP8 and FADD-Like Apoptosis Regulating Protein, pubmed-meshheading:11591744-Carrier Proteins, pubmed-meshheading:11591744-Genes, MHC Class I, pubmed-meshheading:11591744-Humans, pubmed-meshheading:11591744-Intracellular Signaling Peptides and Proteins, pubmed-meshheading:11591744-Jurkat Cells, pubmed-meshheading:11591744-Killer Cells, Natural, pubmed-meshheading:11591744-Membrane Glycoproteins, pubmed-meshheading:11591744-Mice, pubmed-meshheading:11591744-Mice, Mutant Strains, pubmed-meshheading:11591744-Neoplasm Transplantation, pubmed-meshheading:11591744-Perforin, pubmed-meshheading:11591744-Pore Forming Cytotoxic Proteins, pubmed-meshheading:11591744-Receptors, Tumor Necrosis Factor, pubmed-meshheading:11591744-Signal Transduction, pubmed-meshheading:11591744-Transplantation Immunology
pubmed:year
2001
pubmed:articleTitle
Inhibition of the death receptor pathway by cFLIP confers partial engraftment of MHC class I-deficient stem cells and reduces tumor clearance in perforin-deficient mice.
pubmed:affiliation
Graduate Program in Immunology, and Departments of Pathology, and Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. mesha.taylor@utsouthwestern.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.