Autoimmunity to Myelin Oligodendrocyte Glycoprotein in Rats Mimics the Spectrum of Multiple Sclerosis Pathology
Identifieur interne : 000396 ( Istex/Curation ); précédent : 000395; suivant : 000397Autoimmunity to Myelin Oligodendrocyte Glycoprotein in Rats Mimics the Spectrum of Multiple Sclerosis Pathology
Auteurs : Maria K. Storch [Autriche] ; Andreas Stefferl [Allemagne] ; Uschi Brehm [Allemagne] ; Robert Weissert [Suède] ; Erik Wallström [Suède] ; Martin Kerschensteiner [Allemagne] ; Tomas Olsson [Suède] ; Chris Linington [Allemagne] ; Hans Lassmann [Autriche]Source :
- Brain Pathology [ 1015-6305 ] ; 1998-10.
English descriptors
- Teeft :
- Active demyelination, Allergic encephalomyelitis, Autoimmune, Autoimmune encephalomyelitis, Autoimmunity, Axon, Bielschowsky silver impregnation, Blue myelin stain, Cerebellar, Cerebellar type, Chronic myelin oligodendrocyte glycoprotein, Clinical neurology, Degenerating myelin sheaths, Demyelinated, Demyelinating, Demyelinating antibodies, Demyelinating areas, Demyelinating diseases, Demyelinating lesions, Demyelination, Destructive lesions, Different markers, Encephalomyelitis, Environmental factors, Eosinophilic granulocytes, General neuropathology, Genetic background, Glial fibrillary acidic protein, Glycoprotein, Granulocyte, Immune reactions, Immunocytochemistry, Inflammation, Inflammatory, Lassmann, Lesion, Lesional, Lesional distribution, Luxol, Macrophage, Multiple sclerosis, Myelin, Myelin oligodendrocyte glycoprotein, Myelitis, Neuritis, Neurol, Neuromyelitis, Neuromyelitis optica, Neuropathology, Oligodendrocyte, Optic, Optic nerve, Optic nerve involvement, Optic nerves, Optic neuritis, Optic system, Optica, Periventricular, Periventricular type, Plaque, Plaque distribution, Present study, Proteolipid protein, Rat, Sclerosis, Sensitization, Significant differences, Spinal, Spinal cord, Spinal type, Storch, Subpial demyelination.
Abstract
Multiple sclerosis is a chronic inflammatory disease characterized by perivenous inflammation and focal destruction of myelin. Many attempts have been undertaken previously to create animal models of chronic inflammatory demyelinating diseases through autoimmunity or virus infection. Recently, however, a new model of myelin oligodendrocyte glycoprotein (MOG) induced autoimmune encephalomyelitis became available, which, in a very standardized and predictable way, leads to chronic (relapsing or progressive) disease and widespread CNS demyelination. In the present study we actively induced MOG‐experimental autoimmune encephalomyelitis (EAE) in different inbred rat strains using different immunization protocols. The pathology found in our models closely reflects the spectrum of multiple sclerosis (MS) pathology: Classical MS as well as variants such as optic neuritis, Devic's disease and Marburg's type of acute MS are mimicked in rats immunized with MOG antigen. Furthermore we demonstrate, that by using the proper strain/sensitization regime, subforms of MS such as for instance neuromyelitis optica can be reproducibly induced. Our study further supports the notion, that incidence and expression of the disease in this model, alike the situation in multiple sclerosis, is determined by genetic and environmental factors.
Url:
DOI: 10.1111/j.1750-3639.1998.tb00194.x
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<profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Active demyelination</term>
<term>Allergic encephalomyelitis</term>
<term>Autoimmune</term>
<term>Autoimmune encephalomyelitis</term>
<term>Autoimmunity</term>
<term>Axon</term>
<term>Bielschowsky silver impregnation</term>
<term>Blue myelin stain</term>
<term>Cerebellar</term>
<term>Cerebellar type</term>
<term>Chronic myelin oligodendrocyte glycoprotein</term>
<term>Clinical neurology</term>
<term>Degenerating myelin sheaths</term>
<term>Demyelinated</term>
<term>Demyelinating</term>
<term>Demyelinating antibodies</term>
<term>Demyelinating areas</term>
<term>Demyelinating diseases</term>
<term>Demyelinating lesions</term>
<term>Demyelination</term>
<term>Destructive lesions</term>
<term>Different markers</term>
<term>Encephalomyelitis</term>
<term>Environmental factors</term>
<term>Eosinophilic granulocytes</term>
<term>General neuropathology</term>
<term>Genetic background</term>
<term>Glial fibrillary acidic protein</term>
<term>Glycoprotein</term>
<term>Granulocyte</term>
<term>Immune reactions</term>
<term>Immunocytochemistry</term>
<term>Inflammation</term>
<term>Inflammatory</term>
<term>Lassmann</term>
<term>Lesion</term>
<term>Lesional</term>
<term>Lesional distribution</term>
<term>Luxol</term>
<term>Macrophage</term>
<term>Multiple sclerosis</term>
<term>Myelin</term>
<term>Myelin oligodendrocyte glycoprotein</term>
<term>Myelitis</term>
<term>Neuritis</term>
<term>Neurol</term>
<term>Neuromyelitis</term>
<term>Neuromyelitis optica</term>
<term>Neuropathology</term>
<term>Oligodendrocyte</term>
<term>Optic</term>
<term>Optic nerve</term>
<term>Optic nerve involvement</term>
<term>Optic nerves</term>
<term>Optic neuritis</term>
<term>Optic system</term>
<term>Optica</term>
<term>Periventricular</term>
<term>Periventricular type</term>
<term>Plaque</term>
<term>Plaque distribution</term>
<term>Present study</term>
<term>Proteolipid protein</term>
<term>Rat</term>
<term>Sclerosis</term>
<term>Sensitization</term>
<term>Significant differences</term>
<term>Spinal</term>
<term>Spinal cord</term>
<term>Spinal type</term>
<term>Storch</term>
<term>Subpial demyelination</term>
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<front><div type="abstract" xml:lang="en">Multiple sclerosis is a chronic inflammatory disease characterized by perivenous inflammation and focal destruction of myelin. Many attempts have been undertaken previously to create animal models of chronic inflammatory demyelinating diseases through autoimmunity or virus infection. Recently, however, a new model of myelin oligodendrocyte glycoprotein (MOG) induced autoimmune encephalomyelitis became available, which, in a very standardized and predictable way, leads to chronic (relapsing or progressive) disease and widespread CNS demyelination. In the present study we actively induced MOG‐experimental autoimmune encephalomyelitis (EAE) in different inbred rat strains using different immunization protocols. The pathology found in our models closely reflects the spectrum of multiple sclerosis (MS) pathology: Classical MS as well as variants such as optic neuritis, Devic's disease and Marburg's type of acute MS are mimicked in rats immunized with MOG antigen. Furthermore we demonstrate, that by using the proper strain/sensitization regime, subforms of MS such as for instance neuromyelitis optica can be reproducibly induced. Our study further supports the notion, that incidence and expression of the disease in this model, alike the situation in multiple sclerosis, is determined by genetic and environmental factors.</div>
</front>
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