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JCI Table of Contents, 15 August 2003

h as multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE), an animal model of MS. Danielle Pham-Dinh and colleagues from Hpital de la Salptrire in Paris have generated a mouse lacking a functional Mog gene in order to assess the role of MOG in EAE. In contrast to normal mice, which developed severe EAE following immunization with whole myelin, MOG/ mice had a mild phenotype, demonstrating that the anti-MOG autoimmune response is a major pathogenic component of the anti-myelin immune response. The lack of tolerance to MOG may be responsible for the high level of pathogenicity of the anti-MOG immune response as well as the high susceptibility of most animal strains to EAE induced by MOG. Therefore, immunotherapy aimed at inducing tolerance to MOG might be beneficial in the treatment of MS.

TITLE: Myelin/oligodendrocyte glycoproteindeficient (MOG-deficient) mice reveal lack of immune tolerance to MOG in wild-type mice

AUTHOR CONTACT:
Danielle Pham-Dinh
ISERM Hpital de la Salptrire, Paris, France.
Phone: 33-01-40-77-81-45
Fax: 33-01-40-77-81-17
E-mail: danielle.pham-dinh@chups.jussieu.fr

View the PDF of this article at: https://www.the-jci.org/press/15861.pdf


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Contact: Brooke Grindlinger
science_editor@the-jci.org
212-342-9006
Journal of Clinical Investigation
15-Aug-2003


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