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
✍ Scribed by Maria C. Cid; Jordi Esparza; Manel Juan; Agust́i Miralles; Jaume Ordi; Ramón Vilella; Alvaro Urbano-Márquez; Antoni Gayà; Jordi Vives; Jordi Yagüe
- Publisher
- John Wiley and Sons
- Year
- 1994
- Tongue
- English
- Weight
- 717 KB
- Volume
- 24
- Category
- Article
- ISSN
- 0014-2980
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✦ Synopsis
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 f3l and f32 integrin avidity since (a) CD5O-induced adhesion to endothelial cells was abrogated by simultaneous blocking of f3l-and f3Zmediated adhesion pathways but not by interfering with either one individually, (b) CD50 mAb increased pl integrinmediated 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 f3l or f32 integrins on Tlymphocytes. 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.
* Supported by grants from Fondo de Investigacibn Sanitaria (FIS 9310603 and 9410944).