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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
1994-7-8
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pubmed:abstractText |
Regulated adhesion of T lymphocytes to antigen-presenting cells, endothelial cells and extracellular matrix proteins is crucial in T lymphocyte activation and migration to the sites of injury. In this study, we show that three monoclonal antibodies (mAb) recognizing different epitopes on the CD50 (ICAM-3) molecule increase T lymphocyte adhesion to tumor necrosis factor (TNF)-stimulated human umbilical vein endothelial cells and extracellular matrix proteins. These phenomena are mediated by an increase in beta 1 and beta 2 integrin avidity since (a) CD50-induced adhesion to endothelial cells was abrogated by simultaneous blocking of beta 1- and beta 2-mediated adhesion pathways but not by interfering with either one individually, (b) CD50 mAb increased beta 1 integrin-mediated adhesion to extracellular matrix proteins and to fibronectin-derived synthetic peptides, (c) CD50 mAb enhanced T lymphocyte binding to ICAM-1 transfectants, and (d) CD50 mAb did not modify surface expression patterns of beta 1 or beta 2 integrins on T lymphocytes. Our data suggest that constitutively expressed CD50 (ICAM-3) can play a pivotal role in initiating a cascade of adhesion events which may be crucial in immune activation and in the development of inflammatory lesions.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD18,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD29,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Differentiation,
http://linkedlifedata.com/resource/pubmed/chemical/Cell Adhesion Molecules,
http://linkedlifedata.com/resource/pubmed/chemical/Fibronectins,
http://linkedlifedata.com/resource/pubmed/chemical/ICAM3 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Integrins,
http://linkedlifedata.com/resource/pubmed/chemical/Intercellular Adhesion Molecule-1
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0014-2980
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
24
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1377-82
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pubmed:dateRevised |
2008-6-13
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pubmed:meshHeading |
pubmed-meshheading:7515813-Antigens, CD,
pubmed-meshheading:7515813-Antigens, CD18,
pubmed-meshheading:7515813-Antigens, CD29,
pubmed-meshheading:7515813-Antigens, Differentiation,
pubmed-meshheading:7515813-Cell Adhesion,
pubmed-meshheading:7515813-Cell Adhesion Molecules,
pubmed-meshheading:7515813-Cell Aggregation,
pubmed-meshheading:7515813-Cells, Cultured,
pubmed-meshheading:7515813-Endothelium, Vascular,
pubmed-meshheading:7515813-Fibronectins,
pubmed-meshheading:7515813-Flow Cytometry,
pubmed-meshheading:7515813-Humans,
pubmed-meshheading:7515813-Integrins,
pubmed-meshheading:7515813-Intercellular Adhesion Molecule-1,
pubmed-meshheading:7515813-T-Lymphocytes,
pubmed-meshheading:7515813-Umbilical Veins
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pubmed:year |
1994
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pubmed:articleTitle |
Signaling through CD50 (ICAM-3) stimulates T lymphocyte binding to human umbilical vein endothelial cells and extracellular matrix proteins via an increase in beta 1 and beta 2 integrin function.
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pubmed:affiliation |
Department of Immunology, Hospital Clinic i Provincial, Barcelona, Spain.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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