|
|
 Previous Article | Table of Contents | Next Article 
Functional Interactions Between the Thrombin Receptor and the T-Cell Antigen Receptor in Human T-Cell Lines
David E. Joyce,
Yan Chen,
Rochelle A. Erger,
Gary A. Koretzky, and
Steven R. Lentz
From the Veterans Affairs Medical Center, Iowa City, IA; and the Departments of Internal Medicine and Physiology and Biophysics, University of Iowa College of Medicine, Iowa City, IA.
The proteolytically activated thrombin receptor (TR) is expressed by T lymphocytes, which suggests that thrombin may modulate T-cell activation at sites of hemostatic stress. We examined the relationship between TR function and T-cell activation in the Jurkat human T-cell line and in T-cell lines with defined defects in T-cell antigen receptor (TCR) function. Stimulation with thrombin or the synthetic TR peptide SFLLRN produced intracellular Ca2+ transients in Jurkat cells. As the concentration of TR agonist was increased, peak Ca2+ mobilization increased, but influx of extracellular Ca2+ decreased. TR signaling was enhanced in a TCR-negative Jurkat line and in T-cell lines deficient in the tyrosine kinase lck or the tyrosine phosphatase CD45, both of which are essential for normal TCR function. TCR cross-linking with anti-CD3 IgM desensitized TR signaling in Jurkat cells, but not in CD45-deficient cells. A proteinase-activated receptor (PAR-2)-specific agonist peptide, SLIGKV, produced small Ca2+ transients in both MEG-01 human megakaryocytic cells and Jurkat cells, but was less potent than the TR-specific agonist TFRIFD in both cell types. Like TR signaling, PAR-2 signaling was enhanced in TCR-negative or lck-deficient Jurkat clones. These findings provide evidence for functional cross-talk between proteolytically activated receptors and the TCR.
Blood, Vol. 90 No. 5 (September 1), 1997:
pp. 1893-1901
© 1997 by The American Society of Hematology.
 CiteULike  Connotea  Del.icio.us  Digg  Reddit  Technorati What's this?
This article has been cited by other articles:
|
|
|
|
 
A. Rullier, J. Gillibert-Duplantier, P. Costet, G. Cubel, V. Haurie, C. Petibois, D. Taras, N. Dugot-Senant, G. Deleris, P. Bioulac-Sage, et al.
Protease-activated receptor 1 knockout reduces experimentally induced liver fibrosis
Am J Physiol Gastrointest Liver Physiol,
January 1, 2008;
294(1):
G226 - G235.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. Terada, E. A. B. Kelly, and N. N. Jarjour
Increased Thrombin Activity after Allergen Challenge: A Potential Link to Airway Remodeling?
Am. J. Respir. Crit. Care Med.,
February 1, 2004;
169(3):
373 - 377.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
L. Maulon, S. Guerin, J.-E. Ricci, D. FarahiFar, J.-P. Breittmayer, and P. Auberger
T-Cell Receptor Signaling Pathway Exerts a Negative Control on Thrombin-Mediated Increase in [Ca2+]i and p38 MAPK Activation in Jurkat T Cells: Implication of the Tyrosine Kinase p56Lck
Blood,
June 1, 1998;
91(11):
4232 - 4241.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
