|
|
Blood, 1 December 2004, Vol. 104, No. 12, pp. 3766-3773.
Prepublished online as a Blood First Edition Paper on August 10, 2004; DOI 10.1182/blood-2004-02-0578.
 Previous Article | Table of Contents | Next Article 
PHAGOCYTES
A down-regulatable E-selectin ligand is functionally important for PSGL-1–independent leukocyte–endothelial cell interactions
Renata C. O. Zanardo,
Claudine S. Bonder,
John M. Hwang,
Graciela Andonegui,
Lixin Liu,
Dietmar Vestweber,
Lori Zbytnuik, and
Paul Kubes
From the Department of Physiology and Biophysics, Faculty of Medicine, University of Calgary, Calgary, Alberta, Canada; and Institut für Zellbiologie, Zentrum für Molekularbiologie der Entzündung (ZMBE), Universität Münster and Max-Planck-Institute, Münster, Germany.
P-selectin glycoprotein-1 (PSGL-1) supports P-selectin–dependent rolling in vivo and in vitro. However, controversy exists regarding the importance of PSGL-1–dependent and –independent E-selectin rolling. Using antibodies against PSGL-1 and PSGL-1-/- mice, we demonstrated abolition of P-selectin–dependent rolling but only partial inhibition of E-selectin–mediated rolling in the cremaster microcirculation following local administration of tumor necrosis factor  (TNF-). In vitro studies demonstrated that binding of recombinant mouse E-selectin chimera to PSGL-1-/- neutrophils was dramatically decreased in mice treated systemically but not locally with TNF-. Further, PSGL-1 blockade abolished E-selectin–dependent rolling in wild-type mice following systemic TNF- administration but not local TNF- administration. Together, these data support an E-selectin ligand present on PSGL-1-/- neutrophils that is down-regulatable upon systemic but not local activation. To determine whether the PSGL-1–independent E-selectin ligand was physiologically important, we used a P- and E-selectin–dependent cutaneous contact hypersensitivity model. Binding studies showed no E-selectin ligand down-regulation in this model. The few cells that rolled on E-selectin ligand following PSGL-1 antibody administration or in PSGL-1 deficiency were sufficient to induce profound contact hypersensitivity. In conclusion, E-selectin mediates PSGL-1–dependent and independent rolling and the latter can be down-regulated by systemic activation and can replace PSGL-1 to support the development of inflammation.
 CiteULike  Connotea  Del.icio.us  Digg  Reddit  Technorati What's this?
This article has been cited by other articles:
|
|
|
|
 
E. E. Eriksson
No detectable endothelial- or leukocyte-derived L-selectin ligand activity on the endothelium in inflamed cremaster muscle venules
J. Leukoc. Biol.,
July 1, 2008;
84(1):
93 - 103.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
L. Liu, K. D. Puri, J. M. Penninger, and P. Kubes
Leukocyte PI3K{gamma} and PI3K{delta} have temporally distinct roles for leukocyte recruitment in vivo
Blood,
August 15, 2007;
110(4):
1191 - 1198.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
D. V. Ostanin, K. L. Furr, K. P. Pavlick, L. Gray, C. G. Kevil, D. Shukla, D. D'Souza, J. M. Hoffman, and M. B. Grisham
T cell-associated CD18 but not CD62L, ICAM-1, or PSGL-1 is required for the induction of chronic colitis
Am J Physiol Gastrointest Liver Physiol,
June 1, 2007;
292(6):
G1706 - G1714.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. U. Norman and P. Kubes
CD43, a novel lymphocyte ligand for E-selectin
Blood,
February 15, 2006;
107(4):
1252 - 1252.
[Full Text]
[PDF]
|
|
|
|
|
|
|
R. C. Fuhlbrigge, S. L. King, R. Sackstein, and T. S. Kupper
CD43 is a ligand for E-selectin on CLA+ human T cells
Blood,
February 15, 2006;
107(4):
1421 - 1426.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
