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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.0708422

Received for publication July 17, 2008.
Revised January 6, 2009.
Accepted for publication January 13, 2009.

Article

Transcriptional induction of junctional adhesion molecule-C gene expression in activated T cells

Stephan Immenschuh *@, Srivatsava Naidu *, Triantafyllos Chavakis {dagger}, Heike Beschmann {ddagger}, Ralf J. Ludwig {ddagger}{sect}, and Sentot Santoso *

*Institute for Clinical Immunology and Transfusion Medicine, Justus-Liebig-University Giessen, Giessen, Germany; {dagger}Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA; {ddagger}Department of Dermatology, Johann-Wolfgang-Goethe-University, Frankfurt am Main, Germany; and {sect}Department of Dermatology, University of Lübeck, Lübeck, Germany

@ To whom correspondence should be addressed. E-mail: Immenschuh.Stephan{at}mh-hannover.de.


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Abstract

Junctional adhesion molecule (JAM)-C is an Ig superfamily protein, which is involved in the regulation of various inflammatory and vascular events such as transendothelial leukocyte migration. JAM-C is expressed highly on the surface of endothelial cells and platelets, whereas expression in T lymphocytes is not well studied. To investigate the specific gene regulation of JAM-C in T lymphocytes, we determined JAM-C expression in quiescent and activated human T cells. Treatment with the polyclonal T cell activator PHA increased surface and total JAM-C expression in T cells time- and dose-dependently, as determined by flow cytometry and immunoblot analysis. In contrast, no up-regulation of JAM-A in activated T cells was detectable. The highest level of JAM-C up-regulation by PHA was observed in CD3+forkhead box P3+ and CD4+CD25high T cells. Moreover, TCR activation with combined anti-CD3 and anti-CD28 stimulation induced JAM-C expression in T cells. JAM-C induction occurred at the mRNA level, suggesting a transcriptional regulatory mechanism of JAM-C expression. Accordingly, we studied the regulation of the human JAM-C gene promoter in transiently transfected T cells. Luciferase activity of a JAM-C promoter gene construct with three potential consensus sites for the transcription factor NFAT was induced markedly in activated T cells. Finally, pretreatment with two pharmacological inhibitors of calcineurin, cyclosporin A, and FK-506, but not with MAPK inhibitors, blocked JAM-C induction in activated T cells. In summary, JAM-C is up-regulated in activated human T lymphocytes via a transcriptional mechanism, suggesting a potential role of JAM-C in T cell functions.

Key Words: T lymphocytes • gene regulation • cell activation