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          Institute: MPI für Neurobiologie     Collection: Neuroimmunology     Display Documents



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ID: 127445.0, MPI für Neurobiologie / Neuroimmunology
Myelin/oligodendrocyte glycoprotein-deficient (MOG-deficient) mice reveal lack of immune tolerance to MOG in wild-type mice
Authors:Delarasse, C.; Daubas, P.; Mars, L. T.; Vizler, C.; Litzenburger, Tobias; Iglesias, Antonio; Bauer, Jan; Della Gaspera, B.; Schubart, Anna; Decker, L.; Dimitri, D.; Roussel, G.; Dierich, A.; Amor, S.; Dautigny, A.; Liblau, Roland; Pham-Dinh, D.
Language:English
Date of Publication (YYYY-MM-DD):2003-08
Title of Journal:Journal of Clinical Investigation
Journal Abbrev.:J. Clin. Invest.
Volume:112
Issue / Number:4
Start Page:544
End Page:553
Review Status:Peer-review
Audience:Not Specified
Abstract / Description:We studied the immunological basis for the very potent encephalitogenicity of myelin/oligodendrocyte glycoprotein (MOG), a minor component of myelin in the CNS that is widely used to induce experimental autoimmune encephalomyelitis (EAE). For this purpose, we generated a mutant mouse lacking a functional mog gene. This MOG-deficient mouse presents no clinical or histological abnormalities, permitting us to directly assess the role of MOG as a target autoantigen in EAE. In contrast to WT mice, which developed severe EAE following immunization with whole myelin, MOG-deficient mice had a mild phenotype, demonstrating that the anti-MOG response is a major pathogenic component of the autoimmune response directed against myelin. Moreover, while MOG transcripts are expressed in lymphoid organs in minute amounts, both MOG-deficient and V/T mice show similar T and B cell responses against the extracellular domain of MOG, including the immunodominant MOG 35-55 T cell epitope. Furthermore, no differences in the fine specificity of the T cell responses to overlapping peptides covering the complete mouse MOG sequence were observed between MOG(+)/(+) and MOG(-)/(-) mice. In addition, upon adoptive transfer, MOG-specific T cells from WT mice and those from MOG-deficient mice are equally pathogenic. This total lack of immune tolerance to MOG in WT C57BL/6 mice may be responsible for the high pathogenicity of the anti-MOG immune response as well as the high susceptibility of most animal strains to MOG-induced EAE.
Comment of the Author/Creator:Date: 2003, AUG
External Publication Status:published
Document Type:Article
Affiliations:MPI für Neurobiologie/Neuroimmunology (Wekerle)
External Affiliations:Hop La Pitie Salpetriere, INSERM, U546, F-75013 Paris, France.; Max Planck Inst Neurobiol, Martinsried, Germany.; Univ Vienna, Div Neuroimmunol, Brain Res Inst, Vienna, Austria.; Ctr Neurochim, F-67084 Strasbourg, France.; Univ Strasbourg 1, Inst Genet & Biol Mol & Cellulaire, Ctr Natl Rech Sci, INSERM, Illkirch Graffenstaden, France.; Univ London Imperial Coll Sci Technol & Med, Fac Med, London, England.; Biomed Primate Res Ctr, Dept Immunobiol, Rijswijk, Netherlands.
Identifiers:ISI:000184833900014 [ID No:1]
ISSN:0021-9738 [ID No:2]
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