Cell surface CCR5 density determines the intensity of T cell migration towards rheumatoid arthritis synoviocytes

As we have recently shown that the number of CCR5 molecules at the cell surface determines the efficiency of its function as a chemokine receptor, we tested the hypothesis that cell surface CCR5 density could influence the intensity of T lymphocyte recruitment into the rheumatoid joint. For this pur...

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Veröffentlicht in:Clinical immunology (Orlando, Fla.). - 1999. - 123(2007), 2 vom: 23. Mai, Seite 148-54
1. Verfasser: Desmetz, Caroline (VerfasserIn)
Weitere Verfasser: Lin, Yea-Lih, Mettling, Clément, Portalès, Pierre, Noël, Danièle, Clot, Jacques, Jorgensen, Christian, Corbeau, Pierre
Format: Aufsatz
Sprache:English
Veröffentlicht: 2007
Zugriff auf das übergeordnete Werk:Clinical immunology (Orlando, Fla.)
Schlagworte:Journal Article Antibodies, Monoclonal CCL5 protein, human CXCL12 protein, human Chemokine CCL5 Chemokine CXCL12 Chemokines, CC Chemokines, CXC Culture Media, Conditioned Receptors, CCR5 mehr... Receptors, CXCR4 Tumor Necrosis Factor-alpha
Beschreibung
Zusammenfassung:As we have recently shown that the number of CCR5 molecules at the cell surface determines the efficiency of its function as a chemokine receptor, we tested the hypothesis that cell surface CCR5 density could influence the intensity of T lymphocyte recruitment into the rheumatoid joint. For this purpose, we established two Jurkat cell line-derived clones that differed only by their cell surface CCR5 densities. We studied their chemotaxis towards TNF-alpha-transduced rheumatoid synoviocytes supernatant. The Jurkat cell subline that expressed the higher cell surface CCR5 density migrated more intensively towards the supernatant of TNF-alpha-transduced synoviocytes than the Jurkat cell subline that expressed a lower surface CCR5 density. Moreover, this migration was blocked by an anti-CCR5 mAb. The CCR5 density on T cell surface, which is constant over time for a given individual, but varies drastically from one individual to another, might thus be a factor determining the intensity of joint inflammation in the course of RA
Beschreibung:Date Completed 26.06.2007
Date Revised 15.11.2007
published: Print-Electronic
Citation Status MEDLINE
ISSN:1521-7035