Document Server@UHasselt >
Research >
Research publications >

Please use this identifier to cite or link to this item: http://hdl.handle.net/1942/10714

Title: CNS-targeted LIF Expression Improves Therapeutic Efficacy and Limits Autoimmune-mediated Demyelination in a Model of Multiple Sclerosis.
Authors: SLAETS, Leen
Van den Haute, Chris
Coun, Freya
Baekelandt, Veerle
Issue Date: 2010
Citation: MOLECULAR THERAPY, 18(4). p. 684-691
Abstract: Multiple sclerosis (MS) is a demyelinating disease of the central nervous system (CNS) with an inflammatory and a neurodegenerative component. The neuropoietic cytokine leukemia inhibitory factor (LIF) is expressed in MS lesions, but its effect on lesion development is far from understood. LIF is an interesting candidate for MS therapy, as it has neuroprotective properties and may also promote the survival of myelinating oligodendrocytes (OLGs). However, therapeutic administration of LIF is complicated by its limited ability to cross the blood-brain barrier and its pleiotropic actions outside the CNS. In this study, lentiviral vectors (LVs) were used to achieve stable expression and secretion of LIF in the CNS of adult mice. CNS-targeted expression of LIF significantly reduced demyelination in a murine model of MS. In addition, local expression of LIF ameliorated clinical symptoms with enhanced efficacy compared to systemic treatment with recombinant protein. These findings demonstrate that gene therapeutic administration of LIF is a promising approach to limit lesion burden and clinical symptoms in neuroinflammatory disease.
Notes: Hasselt University, Biomedical Research Institute and transnationale Universiteit Limburg, School of Life Sciences, Diepenbeek, Belgium.
URI: http://hdl.handle.net/1942/10714
DOI: 10.1038/mt.2009.311
ISI #: 000276636800006
ISSN: 1525-0016
Category: A1
Type: Journal Contribution
Validation: ecoom, 2011
Appears in Collections: Research publications

Files in This Item:

Description SizeFormat
Preprint703.99 kBAdobe PDF

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.