Enhancement of central nervous system remyelination in immune and non-immune experimental models of demyelination
Identifieur interne : 001996 ( Main/Exploration ); précédent : 001995; suivant : 001997Enhancement of central nervous system remyelination in immune and non-immune experimental models of demyelination
Auteurs : Baziel Gm Van Engelen [Pays-Bas] ; Kevin D. Pavelko [États-Unis] ; Moses Rodriguez [États-Unis]Source :
- Multiple Sclerosis [ 1352-4585 ] ; 1997-04.
English descriptors
- Teeft :
- Albumin concentration, Animal model, Arch neurol, Autoantibody, Beneficial effect, Cerebrospinal fluid, Clinical improvement, Control group, Delta increase, Demyelinating, Demyelination, Experimental demyelination, Experimental models, Full remyelination, Immune, Immune model, Immune response, Immune system, Immunoglobulin, Ivig, Ivig administration, Ivig treatment, Lysolecithin model, Mayo clinic, Monoclonal antibody, Multiple sclerosis, Myelin, Myelin repair, Neurol, Normal mice, Normal polyclonal, Optic neuritis, Passive transfer, Pathogenic role, Physiological role, Polyclonal, Remyelination, Rodriguez, Sclerosis, Sodium channels, Spinal cord, Spontaneous remyelination, System remyelination, Tmev, Tmev model, Virus model.
Abstract
Studies in both humans and experimental animals indicate that there is potential for full remyelination following CNS demyelination, but the factors that control the degree of myelin repair are unknown. In the Theiler's virus model of demyelination CNS remyelination can be promoted either by global immunosuppression or by selective immunoglobulin therapy. In this paper we discuss whether immunoglobulin-mediated remyelination is a characteristic of immune-mediated demyelination, or whether immunoglobulin-mediated remyelination also occurs in the toxic-traumatic model of lysolecithin-induced demyelination. Our data support the hypothesis that even in a non-primary immune model of demyelination, manipulating the immune system can be beneficial in myelin repair.
Url:
DOI: 10.1177/135245859700300203
Affiliations:
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Le document en format XML
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<sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Enhancement of central nervous system remyelination in immune and non-immune experimental models of demyelination</title>
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<series><title level="j">Multiple Sclerosis</title>
<idno type="ISSN">1352-4585</idno>
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<pubPlace>Sage CA: Thousand Oaks, CA</pubPlace>
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<term>Animal model</term>
<term>Arch neurol</term>
<term>Autoantibody</term>
<term>Beneficial effect</term>
<term>Cerebrospinal fluid</term>
<term>Clinical improvement</term>
<term>Control group</term>
<term>Delta increase</term>
<term>Demyelinating</term>
<term>Demyelination</term>
<term>Experimental demyelination</term>
<term>Experimental models</term>
<term>Full remyelination</term>
<term>Immune</term>
<term>Immune model</term>
<term>Immune response</term>
<term>Immune system</term>
<term>Immunoglobulin</term>
<term>Ivig</term>
<term>Ivig administration</term>
<term>Ivig treatment</term>
<term>Lysolecithin model</term>
<term>Mayo clinic</term>
<term>Monoclonal antibody</term>
<term>Multiple sclerosis</term>
<term>Myelin</term>
<term>Myelin repair</term>
<term>Neurol</term>
<term>Normal mice</term>
<term>Normal polyclonal</term>
<term>Optic neuritis</term>
<term>Passive transfer</term>
<term>Pathogenic role</term>
<term>Physiological role</term>
<term>Polyclonal</term>
<term>Remyelination</term>
<term>Rodriguez</term>
<term>Sclerosis</term>
<term>Sodium channels</term>
<term>Spinal cord</term>
<term>Spontaneous remyelination</term>
<term>System remyelination</term>
<term>Tmev</term>
<term>Tmev model</term>
<term>Virus model</term>
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<front><div type="abstract" xml:lang="en">Studies in both humans and experimental animals indicate that there is potential for full remyelination following CNS demyelination, but the factors that control the degree of myelin repair are unknown. In the Theiler's virus model of demyelination CNS remyelination can be promoted either by global immunosuppression or by selective immunoglobulin therapy. In this paper we discuss whether immunoglobulin-mediated remyelination is a characteristic of immune-mediated demyelination, or whether immunoglobulin-mediated remyelination also occurs in the toxic-traumatic model of lysolecithin-induced demyelination. Our data support the hypothesis that even in a non-primary immune model of demyelination, manipulating the immune system can be beneficial in myelin repair.</div>
</front>
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<country name="États-Unis"><region name="Minnesota"><name sortKey="Pavelko, Kevin D" sort="Pavelko, Kevin D" uniqKey="Pavelko K" first="Kevin D" last="Pavelko">Kevin D. Pavelko</name>
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