rdf:type |
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lifeskim:mentions |
umls-concept:C0021467,
umls-concept:C0021469,
umls-concept:C0024518,
umls-concept:C0026809,
umls-concept:C0027651,
umls-concept:C0038250,
umls-concept:C0301944,
umls-concept:C0392756,
umls-concept:C0449297,
umls-concept:C0456387,
umls-concept:C0728938,
umls-concept:C1704259,
umls-concept:C1705987,
umls-concept:C1720947
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pubmed:issue |
8
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pubmed:dateCreated |
2001-10-9
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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.
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pubmed:grant |
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pubmed:commentsCorrections |
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pubmed:language |
eng
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pubmed:journal |
|
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/CASP8 and FADD-Like Apoptosis...,
http://linkedlifedata.com/resource/pubmed/chemical/CFLAR protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Carrier Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Cflar protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Intracellular Signaling Peptides...,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Glycoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/Perforin,
http://linkedlifedata.com/resource/pubmed/chemical/Pore Forming Cytotoxic Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Tumor Necrosis Factor
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
0022-1767
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pubmed:author |
|
pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
167
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
4230-7
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pubmed:dateRevised |
2007-11-15
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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
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pubmed:year |
2001
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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.
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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
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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