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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.
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Submitted February 19, 2004
Accepted July 25, 2004
A down regulatable E-selectin ligand is functionally important for PSGL-1-independent leukocyte-endothelial cell interactions
Renata C Zanardo, Claudine S Bonder, John M Hwang, Graciela Andonegui, Lixin Liu, Dietmar Vestweber, Lori Zbytnuik, and Paul Kubes*
Department of Physiology and Biophysics, Faculty of Medicine, University of Calgary, Calgary, Alberta, Canada
Institut fur Zellbiologie, Zentrum fur Molekularbiologie der Entzundung (ZMBE), University of Munster and Max-Planck-Institute, Munster, Germany
* Corresponding author; email: pkubes{at}ucalgary.ca.
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 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 which 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.
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