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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
5
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pubmed:dateCreated |
1998-4-9
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pubmed:abstractText |
T lymphocytes react minimally with nonactivated endothelial cells (ECs). However, natural killer (NK) lymphocyte interactions with resting ECs are rapid, avid, and result in endothelial activation and/or cytotoxicity. The molecular basis for these interactions and EC sensitivity to NK-mediated lysis is unclear. To address the EC-specific nature of NK sensitivity, we used syngeneic human umbilical vein ECs, dermal microvascular ECs, dermal fibroblasts, and B lymphoblastoid cell lines in calcein-AM retention NK assays with allogeneic NK effector cells and found the EC lines consistently more NK-sensitive. Because NK inhibitory receptors are engaged by membrane major histocompatibility complex (MHC) I molecules and MHC I-deficient targets are NK-sensitive, we investigated the quantitative levels of membrane MHC I on the panel of syngeneic lines. Highly sensitive ECs expressed similar (or higher) levels of membrane MHC I than their syngeneic NK-resistant counterparts. Pretreatment of ECs with gamma interferon (IFN-gamma) conferred protection against NK-mediated lysis, with much more rapid kinetics (2-6 hr) than those required for membrane MHC I hyperinduction (>8 hr). These kinetics are consistent with induction of transporter associated with antigen processing (TAP) expression and function. As opposed to NK-resistant cell lines, TAP-1 was undetectable in resting ECs. Recombinant expression of the TAP inactivator ICP47 by adenoviral-mediated transduction was used to selectively inhibit IFN-gamma-mediated EC TAP function. ICP47 expression abrogated EC cytoprotection conferred by IFN-gamma. We demonstrate a relationship between both basal and induced TAP-1 expression/function and EC sensitivity to NK-mediated cytotoxicity. We discuss the influence of an induced MHC I-associated peptide repertoire on vascular vulnerability to cytotoxic lymphocytes.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/9482903-1356627,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9482903-1407434,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9482903-1631146,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9482903-1711567,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/9482903-9195970
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0027-8424
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
3
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pubmed:volume |
95
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2435-40
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:9482903-B-Lymphocytes,
pubmed-meshheading:9482903-Carrier Proteins,
pubmed-meshheading:9482903-Cell Membrane,
pubmed-meshheading:9482903-Cells, Cultured,
pubmed-meshheading:9482903-Cytotoxicity, Immunologic,
pubmed-meshheading:9482903-Endothelium, Vascular,
pubmed-meshheading:9482903-Histocompatibility Antigens Class I,
pubmed-meshheading:9482903-Humans,
pubmed-meshheading:9482903-Interferon-gamma,
pubmed-meshheading:9482903-Killer Cells, Natural,
pubmed-meshheading:9482903-Kinetics,
pubmed-meshheading:9482903-Recombinant Proteins,
pubmed-meshheading:9482903-Skin,
pubmed-meshheading:9482903-Transfection,
pubmed-meshheading:9482903-Umbilical Veins
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pubmed:year |
1998
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pubmed:articleTitle |
Induction of transporter associated with antigen processing by interferon gamma confers endothelial cell cytoprotection against natural killer-mediated lysis.
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pubmed:affiliation |
Division of Cardiovascular Medicine and Molecular Cardiobiology, Boyer Center for Molecular Medicine, The Raymond and Beverly Sackler Foundation Cardiobiology Laboratory, Yale University School of Medicine, New Haven, CT 06536-0812, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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