HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Engelhardt, B. Articles by Vestweber, D. Search for Related Content PubMed PubMed Citation Articles by Engelhardt, B. Articles by Vestweber, D.

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.

This article has been cited by other articles:

				A. Doring, M. Wild, D. Vestweber, U. Deutsch, and B. Engelhardt E- and P-Selectin Are Not Required for the Development of Experimental Autoimmune Encephalomyelitis in C57BL/6 and SJL Mice J. Immunol., December 15, 2007; 179(12): 8470 - 8479. [Abstract] [Full Text] [PDF]

				K. Sasaki, X. Zhu, C. Vasquez, F. Nishimura, J. E. Dusak, J. Huang, M. Fujita, A. Wesa, D. M. Potter, P. R. Walker, et al. Preferential Expression of Very Late Antigen-4 on Type 1 CTL Cells Plays a Critical Role in Trafficking into Central Nervous System Tumors Cancer Res., July 1, 2007; 67(13): 6451 - 6458. [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]

				S. M. Kerfoot, M. U. Norman, B. M. Lapointe, C. S. Bonder, L. Zbytnuik, and P. Kubes Reevaluation of P-Selectin and {alpha}4 Integrin as Targets for the Treatment of Experimental Autoimmune Encephalomyelitis J. Immunol., May 15, 2006; 176(10): 6225 - 6234. [Abstract] [Full Text] [PDF]