Accuri C6 Flow Cytometer System
Originally published online as doi:10.1189/jlb.0209117 on August 7, 2009

Published online before print August 7, 2009
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(Journal of Leukocyte Biology. 2009;86:1119-1124.)
© 2009 Society for Leukocyte Biology

PSGL-1-dependent myeloid leukocyte activation

Alexander Zarbock*,{dagger},1, Helena Müller*,{dagger}, Yoshihiro Kuwano{ddagger} and Klaus Ley{ddagger}

* Department of Anesthesiology and Intensive Care Medicine, University of Münster, Münster, Germany;
{dagger} Max-Planck Institute for Molecular Biomedicine, Münster, Germany; and
{ddagger} La Jolla Institute for Allergy and Immunology, La Jolla, California, USA

1. Correspondence: University of Münster, Department of Anesthesiology and Critical Care Medicine, Albert-Schweitzer Str. 33, 48149 Münster, Germany. E-mail: zarbock{at}uni-muenster.de

ABSTRACT

Cell-cell interactions mediating leukocyte recruitment and inflammation are crucial for host defense. Leukocyte recruitment into injured tissue proceeds in a multistep process. The first contact of leukocytes with endothelial cells ("capturing" or "tethering") is mediated by selectins and their counter-receptor P-selectin glyco-protein ligand (PSGL)-1. During capture and rolling, leukocytes collect different inflammatory signals, which can activate various pathways. Integration of these signals leads to leukocyte activation, integrin-mediated arrest, cytoskeleton rearrangement, polarization, and transmigration. PSGL-1 on leukocytes also binds to activated platelets, where P-selectin is expressed at locally high site densities following {alpha}-granule fusion with the plasma membrane. Here, we review the signaling functions of PSGL-1 and speculate how the different known signaling events might relate to different phases of leukocyte recruitment.

Key Words: signaling cascade • integrins • P-selectin glycoprotein ligand 1