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Papers In Press, published online ahead of print January 29, 2001
Centre de Recherche en Infectiologie, RC709, CHUQ, Pavillon CHUL, Ste-Foy, Quebec G1V 4G2
Corresponding Author: michel.j.tremblay{at}crchul.ulaval.ca
Intercellular adhesion molecule 1 (ICAM-1) plays an important role in adhesion phenomena involved in the immune response. The strength of adhesion has been shown to be modulated by changes in ICAM-1 gene expression. In T cells, signaling pathways are intimately regulated by an equilibrium between protein tyrosine kinases (PTK) and protein tyrosine phosphatases (PTP). The use of bis-peroxovanadium (bpV) compounds, a class of potent PTP inhibitors, enabled us to investigate the involvement of phosphotyrosyl phosphatases in the regulation of ICAM-1 gene expression in human T cells. Here, we demonstrate for the first time that inhibition of PTP results in an increase of ICAM-1 surface expression on both human T lymphoid and primary mononuclear cells. The crucial role played by the NF-
J. Biol. Chem, 10.1074/jbc.M005067200
Submitted on June 12, 2000
Revised on January 29, 2001
Accepted on January 26, 2001
Intercellular adhesion molecule-1 (ICAM-1) gene expression in human T cells is regulated by phosphotyrosyl phosphatase activity: involvement of NF-
B, Ets, and pI
RE-binding sites
B-, Ets-, and pI
RE-binding sites in bpV[pic]-mediated activation of ICAM-1 was demonstrated using various 5' deletion and site-specific mutants of the ICAM-1 gene promoter driving the luciferase reporter gene. Co-transfection experiments with trans-dominant mutants and electrophoretic mobility shift assays confirmed the importance of constitutive and inducible transcription factors that bind to specific responsive elements in bpV-dependent upregulation of ICAM-1 surface expression. Altogether, these observations suggest that expression of ICAM-1 in human T cells is regulated by phosphotyrosyl phosphatase activity through NF-B-, Ets-, and STAT-1-dependent signaling pathways.
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