Editorial: PSGL-1—the hidden player in T cell trafficking into the brain in multiple sclerosis? Britta Engelhardt 1 Theodor Kocher Institute, University of Bern, Bern, Switzerland 1. Correspondence: Theodor Kocher Institute, University of Bern, Freiestrasse 1, CH-3012 Bern, Switzerland. E-mail: bengel@tki.unibe.ch cellular immunology cell adhesion blood-brain barrier experimental autoimmune encephalomyelitis In MS, a large number of inflammatory cells gain access to the CNS parenchyma, causing inflammation, BBB breakdown, and demyelination, which all pave the way to the development of clinical manifestations of this disabling disease. Studies performed in EAE, a CD4 T cell-mediated rodent model for MS, have helped to elucidate some of the molecular mechanisms involved in immune cell entry into the CNS. In particular, the realization that α4-integrins play a predominant role in T cell trafficking into the CNS in EAE has led to the development of a humanized anti-α4-integrin antibody as a novel treatment of relapsing-remitting MS [ 1 ] . By visualizing the CNS microvasculature using intravital microscopy, it was shown that this antibody specifically inhibits the firm adhesion but not the rolling or capture of human T cells to the inflamed BBB in vivo [ 2 ] . Thus, the roles of other adhesion
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Editorial: PSGL-1—the hidden player in T cell trafficking into the brain in multiple sclerosis?
Engelhardt, Britta
Follow Journal of Leukocyte Biology
, Volume 86 (5): 1023
Fed of American Socs for Experimental Biology – Nov 1, 2009
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