Mechanism of TREK1-mediated T lymphocyte transmigration via the blood-brain-barrier

TREK1 is expressed on endothelial cells in the CNS and downregulated in inflammatory lesions of MS patients.
© Stefan Bittner, Thomas Budde, Petra Ehling, Sven Meuth, Heinz Wiendl

Principal investigators: Stefan Bittner, Thomas Budde, Petra Ehling, Sven Meuth, Heinz Wiendl
Project time: 07/2014 - 06/2016
Project code: FF-2014-05

Multiple Sclerosis is a chronic inflammatory demyelinating autoimmune disease of the central nervous system. Autoreactive T lymphocytes which have to cross the activated blood-brain-barrier (BBB) play an important role in its pathogenesis. We recently analysed the phenotype of genetic deletion of TREK1 (Trek1-/- mice) focusing on the immunological phenotype of brain endothelial cells in vitro and in animal models of neuroinflammation in vivo. In the current project, we aim to investigate the molecular mechanisms that underlie the stabilization of BBB integrity by TREK1 ion channels.