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Predicate | Object |
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rdf:type | |
lifeskim:mentions |
umls-concept:C0019721,
umls-concept:C0022567,
umls-concept:C0024348,
umls-concept:C0039194,
umls-concept:C0039195,
umls-concept:C0063695,
umls-concept:C0064830,
umls-concept:C0079091,
umls-concept:C0079717,
umls-concept:C0086418,
umls-concept:C0086597,
umls-concept:C0456387,
umls-concept:C1515895,
umls-concept:C2349975
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pubmed:issue |
7
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pubmed:dateCreated |
1991-4-22
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pubmed:abstractText |
Exposure of human KC to IFN-gamma increases their susceptibility to lysis by CTL. The mechanism of this enhanced lysis was investigated by analyzing interactions of IFN-gamma-treated and nontreated cultured KC with allogeneic class I-specific CTL clones. rIFN-gamma treatment augmented KC lysis in a time- and dose-dependent manner. Increased lysis of IFN-KC was detected after only 2 h of IFN-gamma treatment and was maximal by 12 h. Enhanced lysis of IFN-KC was Ag-specific, inasmuch as nonantigenic IFN-KC were not lysed either directly or as bystanders during the lysis of antigenic KC. Parallel immunofluorescence and cytotoxicity assays of KC treated with IFN-gamma for various intervals revealed a direct correlation between the degree of increased KC lysis and levels of cell surface ICAM-1 (CD54), but not of specific alloantigen or beta 2-microglobulin. Lysis of nontreated KC was blocked by mAb against class I or CD3, but not by mAb against ICAM-1 or LFA-1. In contrast, lysis of IFN-KC was partially inhibited by anti-ICAM-1 or anti-LFA-1 mAb, but resisted inhibition by anti-class I mAb except in the presence of anti-ICAM-1. These results indicate that both ICAM-1/LFA-1 and Ag/CD3-TcR interactions are important for Ag-specific lysis of IFN-KC, whereas lysis of nontreated KC depends on Ag/CD3-TcR but not ICAM-1/LFA-1 interactions. Equivalent inhibition of IFN-KC lysis by mAb against ICAM-1 or LFA-1 suggests that ICAM-1 is the only LFA-1 ligand involved in enhanced IFN-KC lysis. Furthermore, enhanced CTL lysis of KC after short-term IFN-gamma treatment can be explained solely on the basis of ICAM-1 induction, because all of the increase in specific lysis associated with IFN-gamma treatment could be blocked by mAb that block ICAM-1/LFA-1 interactions.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Cell Adhesion Molecules,
http://linkedlifedata.com/resource/pubmed/chemical/Histocompatibility Antigens Class I,
http://linkedlifedata.com/resource/pubmed/chemical/Intercellular Adhesion Molecule-1,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma,
http://linkedlifedata.com/resource/pubmed/chemical/Lymphocyte Function-Associated...,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Proteins
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
0022-1767
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
146
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2169-75
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:1672345-Cell Adhesion Molecules,
pubmed-meshheading:1672345-Cells, Cultured,
pubmed-meshheading:1672345-Cytotoxicity, Immunologic,
pubmed-meshheading:1672345-Dose-Response Relationship, Drug,
pubmed-meshheading:1672345-Dose-Response Relationship, Immunologic,
pubmed-meshheading:1672345-Histocompatibility Antigens Class I,
pubmed-meshheading:1672345-Humans,
pubmed-meshheading:1672345-Immunity, Cellular,
pubmed-meshheading:1672345-Intercellular Adhesion Molecule-1,
pubmed-meshheading:1672345-Interferon-gamma,
pubmed-meshheading:1672345-Keratinocytes,
pubmed-meshheading:1672345-Lymphocyte Function-Associated Antigen-1,
pubmed-meshheading:1672345-Recombinant Proteins,
pubmed-meshheading:1672345-T-Lymphocytes, Cytotoxic
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pubmed:year |
1991
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pubmed:articleTitle |
Lysis of human keratinocytes by allogeneic HLA class I-specific cytotoxic T cells. Keratinocyte ICAM-1 (CD54) and T cell LFA-1 (CD11a/CD18) mediate enhanced lysis of IFN-gamma-treated keratinocytes.
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pubmed:affiliation |
Clinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98104.
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pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, U.S. Gov't, P.H.S.
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