Klein

Robyn Klein, MD, PhD

Associate Professor of Medicine

Cellular and molecular studies of viral and autoimmune encephalitides Read More

Email: rklein@id.wustl.edu
Lab Phone: (314) 286-2137
Website: Klein Lab
Lab Location: McDonnell Pediatric Research Building 7273
Keywords: roles of inflammatory mediators in protection and repair of the CNS during viral and autoimmune encephalitides, neuroinflammatory murine models using in vivo pharmacologic inhibition or RNA silencing, in vitro models of the blood-brain barrier

Cellular and molecular studies of viral and autoimmune encephalitides

Immune cells (green) remain in the meninges (delineated by arrows) in CXCR7 antagonist-treated animals versus those treated with vehicle

My laboratory studies the pathogenesis of neuroinflammatory diseases of the central nervous system (CNS). We have focused on two components of CNS inflammatory states: the mechanism of leukocyte recruitment into the CNS and the direct effects of inflammatory mediators on resident neural cells. Common to both of these is the action of chemokines, which both recruit leukocytes into the CNS and signal through chemokine receptors present on neural cells, affecting their function and survival. Our experimental approach involves the development of in vitro and in vivo models of CNS mononuclear cell recruitment and neural cell chemokine receptor signaling responses. Our studies over the past few years have led us to focus on the roles of cytokines and chemokines in the regulation of blood-brain barrier permeability to protective versus pathogenic leukocytes, and to West Nile virus (WNV), a positive strand flavivirus that may enter the CNS and cause encephalitis. These inflammatory cues also regulate CNS repair by neural progenitor cells (NPCs) in mice with viral infection or demyelinating diseases. Aspects related to NPC-mediated repair include defining the localizing, proliferative and differentiation cues that lead to successful repair of damaged neurons and myelin.


Updated February 2014

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