The Journal of Experimental Medicine
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Published online 15 May 2000.
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© The Rockefeller University Press, 0022-1007/2000/5/1799/ $5.00
The Journal of Experimental Medicine, Volume 191, Number 10, May 15, 2000 1799-1806

Brief Definitive Report

Human Nerve Growth Factor Protects Common Marmosets against Autoimmune Encephalomyelitis by Switching the Balance of T Helper Cell Type 1 and 2 Cytokines within the Central Nervous System

Pablo Villosladaa,c, Stephen L. Hausera, Ilse Bartked, Jurgen Ungere, Nathan Healda, Daniel Rosenberga, Steven W. Cheungb, William C. Mobleya, Stefan Fisherd, and Claude P. Genaina

a Department of Neurology, University of California at San Francisco, San Francisco, California 94143-0435
b Department of Otolaryngology, University of California at San Francisco, San Francisco, California 94143-0435
c Neuroimmunology Unit, Hospital Vall d'Hebron, 08035 Barcelona, Spain
d Pharma Research Penzberg, Roche Diagnostics GmbH, 82372 Penzberg, Germany
e Department of Anatomy, Ludwig-Maximilians-Universität, Munich 80336, Germany
Department of Neurology, University of California, 513 Parnassus Ave., Rm. C-440, San Francisco, CA 94143-0435.415-502-5899415-502-5684

claudeg{at}itsa.ucsf.edu

Multiple sclerosis is a demyelinating disorder of the central nervous system (CNS), in which an immune attack directed against myelin constituents causes myelin destruction and death of oligodendrocytes, the myelin-producing cells. Here, the efficacy of nerve growth factor (NGF), a growth factor for neurons and oligodendrocytes, in promoting myelin repair was evaluated using the demyelinating model of experimental allergic encephalomyelitis (EAE) in the common marmoset. Surprisingly, we found that NGF delayed the onset of clinical EAE and, pathologically, prevented the full development of EAE lesions. We demonstrate by immunocytochemistry that NGF exerts its antiinflammatory effect by downregulating the production of interferon {gamma} by T cells infiltrating the CNS, and upregulating the production of interleukin 10 by glial cells in both inflammatory lesions of EAE and normal-appearing CNS white matter. Thus, NGF, currently under investigation in human clinical trials as a neuronal trophic factor, may be an attractive candidate for therapy of autoimmune demyelinating disorders.

Key Words: multiple sclerosis • nonhuman primate • interferon {gamma} • interleukin 10 • growth factors

© 2000 The Rockefeller University Press


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