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P-Selectin Glycoprotein Ligand 1 Is Not Required for the Development of Experimental Autoimmune Encephalomyelitis in SJL and C57BL/6 Mice¹

Britta Engelhardt^2,*,, Birgit Kempe, Stephanie Merfeld-Clauss, Melanie Laschinger, Bruce Furie, Martin K. Wild and Dietmar Vestweber^,

^* Theodor Kocher Institute, University of Bern, Bern, Switzerland; Max-Planck Institute for Molecular Biomedicine and Institute for Cell Biology, Zentrum für Molekularbiologie der Entzündung, Münster, Germany; and Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02215

In multiple sclerosis and in its animal model experimental autoimmune encephalomyelitis (EAE), inflammatory cells migrate across the endothelial blood-brain barrier and gain access to the CNS. The involvement of P-selectin glycoprotein ligand 1 (PSGL-1) and of its major endothelial ligand P-selectin in this process have been controversial. In this study we demonstrate that although encephalitogenic T cells express functional PSGL-1, which can bind to soluble and immobilize P-selectin if presented in high concentrations, PSGL-1 is not involved T cell interaction with P-selectin expressing brain endothelial cells in vitro. Furthermore, neither anti-PSGL-1 Abs nor the lack of PSGL-1 in PSGL-1-deficient mice inhibits the recruitment of inflammatory cells across the blood-brain barrier or the development of clinical EAE. Taken together, our findings demonstrate that PSGL-1 is not required for the pathogenesis of EAE.

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