The N-terminal domain of the myelin oligodendrocyte glycoprotein (MOG) induces acute demyelinating experimental autoimmune encephalomyelitis in the Lewis rat

Adelmann, Martin; Wood, John C.; Benzel, Isabel; Fiori, P.; Lassmann, Hans; Matthieu, Jean‐Marie; Gardinier, Minnetta V.; Dornmair, Klaus; Linington, Christopher

doi:10.1016/0165-5728(95)00124-7

Cited by 221 publications

(152 citation statements)

References 21 publications

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“…These possibilities are not mutually exclusive. Moreover, anti-MOG antibodies directed against conformational epitopes have been shown to mediate antibody-mediated demyelination; 53,54 thus, being consistent with the first option. It is generally accepted that the IgG isotype profile reflects the underlying cytokine environment in EAE.…”

Section: Eae-regulating Qtls On Rn04 M Marta Et Almentioning

confidence: 79%

Multiple loci comprising immune-related genes regulate experimental neuroinflammation

et al. 2009

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A 58 Mb region on rat chromosome 4 known to regulate experimental autoimmune encephalomyelitis (EAE) was genetically dissected. High-resolution linkage analysis in an advanced intercross line (AIL) revealed four quantitative trait loci (QTLs), Eae24-Eae27. Both Eae24 and Eae25 regulated susceptibility and severity phenotypes, whereas Eae26 regulated severity and Eae27 regulated susceptibility. Analyses of the humoral immune response revealed that the levels of serum anti-myelin oligodendrocyte glycoprotein (MOG) immunoglobin G1 (IgG1) antibodies are linked to Eae24 and anti-MOG IgG2b antibodies are linked to both Eae24 and Eae26. We tested the parental DA strain and six recombinant congenic strains that include overlapping fragments of this region in MOG-EAE. Eae24 and Eae25 showed significant protection during the acute phase of EAE, whereas Eae25 and Eae26 significantly modified severity but not susceptibility. The smallest congenic fragment, which carries Eae25 alone, influenced both susceptibility and severity, and protected from the chronic phase of disease. These results support the multiple QTLs identified in the AIL. By demonstrating several QTLs comprising immune-related genes, which potentially interact, we provide a significant step toward elucidation of the polygenically regulated pathogenesis of MOG-EAE and possibly multiple sclerosis (MS), and opportunities for comparative genetics and testing in MS case-control cohorts.

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Section: Eae-regulating Qtls On Rn04 M Marta Et Almentioning

confidence: 79%

Multiple loci comprising immune-related genes regulate experimental neuroinflammation

et al. 2009

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“…Other features of optic neuritis in EAE include optic disc oedema, cellular infiltrate that predominantly involves the retrobulbar optic nerve, and blood-brain barrier disruption. It is now believed that immunization with MOG produces a chronic form of EAE, referred to as chronic relapsing EAE, in which animals go through multiple episodes of relapses and remissions, a clinical picture that better mimics MS. 38,39 Furthermore, it has been demonstrated that by using different immunization protocols and proper rat strains subforms of MS can be reproducibly induced. 40 EAE can be induced in a number of experimental laboratory animals, including primates, rats, and mice.…”

Section: Experimental Model For Optic Neuritismentioning

confidence: 99%

Animal models of optic nerve diseases

Levkovitch-Verbin

2004

Eye

115

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“…These studies imply that MOG peptide-specific antibodies and/or anti-MOG serum may be pathogenic in this strain, as it seems to be the case in several mouse and rat strains (Bernard et al, 1997). According to some (Ichikawa et al, 1996a) but not all (Adelmann et al, 1995) investigations, Lewis rats immunized with MOG 35-55 can develop multifocal demyelinating disease despite the demonstration that these animals do not develop conformation-dependent anti-MOG antibodies (Ichikawa et al, 1996a(Ichikawa et al, , 1996b.…”

Section: Introductionmentioning

confidence: 99%

Antibody response in MOG35–55 induced EAE

Lalive

Molnarfi

Benkhoucha

et al. 2011

Journal of Neuroimmunology

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Neurological deficit in experimental autoimmune encephalomyelitis (EAE) and multiple sclerosis is widely considered to be a consequence of synergistic T and B cell responses to central nervous system (CNS) antigens. We show that mice immunized with encephalitogenic myelin oligodendrocyte glycoprotein ) peptide develop significant serum levels of anti-MOG antibodies in parallel with disease progression. Furthermore, EAE mice developed antibodies against DNA and RNA, a serological hallmark observed in autoimmune diseases such as systemic lupus erythematosus. The presence of anti-nucleic responsive B cells and antibodies during EAE may highlight a previously unappreciated mechanism in the pathogenesis of CNS autoimmunity.

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The N-terminal domain of the myelin oligodendrocyte glycoprotein (MOG) induces acute demyelinating experimental autoimmune encephalomyelitis in the Lewis rat

Cited by 221 publications

References 21 publications

Multiple loci comprising immune-related genes regulate experimental neuroinflammation

Multiple loci comprising immune-related genes regulate experimental neuroinflammation

Animal models of optic nerve diseases

Antibody response in MOG35–55 induced EAE

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