Signaling through CD50 (ICAM-3) stimulates T lymphocyte binding to human umbilical vein endothelial cells and extracellular matrix proteins via an increase in β1 and β2 integrin function

Autor: Jordi Esparza, Ramon Vilella, Agust́i Miralles, Antoni Gayà, Maria C. Cid, Jaume Ordi, Alvaro Urbano-Márquez, Jordi Vives, Manel Juan, Jordi Yagüe
Rok vydání: 1994
Předmět:
Zdroj: European Journal of Immunology. 24:1377-1382
ISSN: 1521-4141
0014-2980
DOI: 10.1002/eji.1830240621
Popis: 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.
Databáze: OpenAIRE