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J Neuroimmunol. 2012 Oct 15;251(1-2):14-24. doi: 10.1016/j.jneuroim.2012.06.005. Epub 2012 Jun 28.

Oral treatment with laquinimod augments regulatory T-cells and brain-derived neurotrophic factor expression and reduces injury in the CNS of mice with experimental autoimmune encephalomyelitis.

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  • 1Department of Immunology, The Weizmann Institute of Science, Rehovot, Israel. rina.aharoni@weizmann.ac.il

Abstract

Laquinimod is an orally active molecule that showed efficacy in clinical trials in multiple sclerosis. We studied its effects in the CNS, when administered by therapeutic regimen to mice inflicted with experimental autoimmune encephalomyelitis (EAE). Laquinimod reduced clinical and inflammatory manifestations and elevated the prevalence of T-regulatory cells in the brain. In untreated mice, in the chronic disease stage, brain derived neurotrophic factor (BDNF) expression was impaired. Laquinimod treatment restored BDNF expression to its level in healthy controls. Furthermore, CNS injury, manifested by astrogliosis, demyelination and axonal damages, was significantly reduced following laquinimod treatment, indicating its immunomodulatory and neuroprotective activity.

Copyright © 2012 Elsevier B.V. All rights reserved.

PMID:
22749337
[PubMed - indexed for MEDLINE]
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