Autoimmunity to Myelin Oligodendrocyte Glycoprotein in Rats Mimics the Spectrum of Multiple Sclerosis Pathology
Identifieur interne : 000429 ( Istex/Corpus ); précédent : 000428; suivant : 000430Autoimmunity to Myelin Oligodendrocyte Glycoprotein in Rats Mimics the Spectrum of Multiple Sclerosis Pathology
Auteurs : Maria K. Storch ; Andreas Stefferl ; Uschi Brehm ; Robert Weissert ; Erik Wallström ; Martin Kerschensteiner ; Tomas Olsson ; Chris Linington ; Hans LassmannSource :
- 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
Links to Exploration step
ISTEX:289D82BFB5AAD1E0F90AD378A31CC4E77A71CBC7Le document en format XML
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Storch</name><affiliation><mods:affiliation>Neurological Institute, University of Vienna, A‐1090 Vienna, Austria</mods:affiliation></affiliation></author><author><name sortKey="Stefferl, Andreas" sort="Stefferl, Andreas" uniqKey="Stefferl A" first="Andreas" last="Stefferl">Andreas Stefferl</name><affiliation><mods:affiliation>Max‐Planck‐Insitute for Neurobiology, D‐82152 Martinsried, Germany</mods:affiliation></affiliation></author><author><name sortKey="Brehm, Uschi" sort="Brehm, Uschi" uniqKey="Brehm U" first="Uschi" last="Brehm">Uschi Brehm</name><affiliation><mods:affiliation>Max‐Planck‐Insitute for Neurobiology, D‐82152 Martinsried, Germany</mods:affiliation></affiliation></author><author><name sortKey="Weissert, Robert" sort="Weissert, Robert" uniqKey="Weissert R" first="Robert" last="Weissert">Robert Weissert</name><affiliation><mods:affiliation>Neuroimmunology Unit, Center of Molecular Medicine, Karolinska Hospital, S‐17176 Stockholm, Sweden</mods:affiliation></affiliation></author><author><name sortKey="Wallstrom, Erik" sort="Wallstrom, Erik" uniqKey="Wallstrom E" first="Erik" last="Wallström">Erik Wallström</name><affiliation><mods:affiliation>Neuroimmunology Unit, Center of Molecular Medicine, Karolinska Hospital, S‐17176 Stockholm, Sweden</mods:affiliation></affiliation></author><author><name sortKey="Kerschensteiner, Martin" sort="Kerschensteiner, Martin" uniqKey="Kerschensteiner M" first="Martin" last="Kerschensteiner">Martin Kerschensteiner</name><affiliation><mods:affiliation>Max‐Planck‐Insitute for Neurobiology, D‐82152 Martinsried, Germany</mods:affiliation></affiliation></author><author><name sortKey="Olsson, Tomas" sort="Olsson, Tomas" uniqKey="Olsson T" first="Tomas" last="Olsson">Tomas Olsson</name><affiliation><mods:affiliation>Neuroimmunology Unit, Center of Molecular Medicine, Karolinska Hospital, S‐17176 Stockholm, Sweden</mods:affiliation></affiliation></author><author><name sortKey="Linington, Chris" sort="Linington, Chris" uniqKey="Linington C" first="Chris" last="Linington">Chris Linington</name><affiliation><mods:affiliation>Max‐Planck‐Insitute for Neurobiology, D‐82152 Martinsried, Germany</mods:affiliation></affiliation></author><author><name sortKey="Lassmann, Hans" sort="Lassmann, Hans" uniqKey="Lassmann H" first="Hans" last="Lassmann">Hans Lassmann</name><affiliation><mods:affiliation>Neurological Institute, University of Vienna, A‐1090 Vienna, Austria</mods:affiliation></affiliation><affiliation><mods:affiliation>Correspondence address: Corresponding Author: Prof. Dr. Hans Lassmann, Institute of Neurology, University of Vienna, Schwarzspanierstrasse 17, A‐1090 Vienna; Tel.: (431) 427796–11; Fax: (431) 4277 97 96</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:289D82BFB5AAD1E0F90AD378A31CC4E77A71CBC7</idno><date when="1998" year="1998">1998</date><idno type="doi">10.1111/j.1750-3639.1998.tb00194.x</idno><idno type="url">https://api.istex.fr/ark:/67375/WNG-FWL8W1CK-Z/fulltext.pdf</idno><idno type="wicri:Area/Istex/Corpus">000429</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">000429</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main">Autoimmunity to Myelin Oligodendrocyte Glycoprotein in Rats Mimics the Spectrum of Multiple Sclerosis Pathology</title><author><name sortKey="Storch, Maria K" sort="Storch, Maria K" uniqKey="Storch M" first="Maria K." last="Storch">Maria K. Storch</name><affiliation><mods:affiliation>Neurological Institute, University of Vienna, A‐1090 Vienna, Austria</mods:affiliation></affiliation></author><author><name sortKey="Stefferl, Andreas" sort="Stefferl, Andreas" uniqKey="Stefferl A" first="Andreas" last="Stefferl">Andreas Stefferl</name><affiliation><mods:affiliation>Max‐Planck‐Insitute for Neurobiology, D‐82152 Martinsried, Germany</mods:affiliation></affiliation></author><author><name sortKey="Brehm, Uschi" sort="Brehm, Uschi" uniqKey="Brehm U" first="Uschi" last="Brehm">Uschi Brehm</name><affiliation><mods:affiliation>Max‐Planck‐Insitute for Neurobiology, D‐82152 Martinsried, Germany</mods:affiliation></affiliation></author><author><name sortKey="Weissert, Robert" sort="Weissert, Robert" uniqKey="Weissert R" first="Robert" last="Weissert">Robert Weissert</name><affiliation><mods:affiliation>Neuroimmunology Unit, Center of Molecular Medicine, Karolinska Hospital, S‐17176 Stockholm, Sweden</mods:affiliation></affiliation></author><author><name sortKey="Wallstrom, Erik" sort="Wallstrom, Erik" uniqKey="Wallstrom E" first="Erik" last="Wallström">Erik Wallström</name><affiliation><mods:affiliation>Neuroimmunology Unit, Center of Molecular Medicine, Karolinska Hospital, S‐17176 Stockholm, Sweden</mods:affiliation></affiliation></author><author><name sortKey="Kerschensteiner, Martin" sort="Kerschensteiner, Martin" uniqKey="Kerschensteiner M" first="Martin" last="Kerschensteiner">Martin Kerschensteiner</name><affiliation><mods:affiliation>Max‐Planck‐Insitute for Neurobiology, D‐82152 Martinsried, Germany</mods:affiliation></affiliation></author><author><name sortKey="Olsson, Tomas" sort="Olsson, Tomas" uniqKey="Olsson T" first="Tomas" last="Olsson">Tomas Olsson</name><affiliation><mods:affiliation>Neuroimmunology Unit, Center of Molecular Medicine, Karolinska Hospital, S‐17176 Stockholm, Sweden</mods:affiliation></affiliation></author><author><name sortKey="Linington, Chris" sort="Linington, Chris" uniqKey="Linington C" first="Chris" last="Linington">Chris Linington</name><affiliation><mods:affiliation>Max‐Planck‐Insitute for Neurobiology, D‐82152 Martinsried, Germany</mods:affiliation></affiliation></author><author><name sortKey="Lassmann, Hans" sort="Lassmann, Hans" uniqKey="Lassmann H" first="Hans" last="Lassmann">Hans Lassmann</name><affiliation><mods:affiliation>Neurological Institute, University of Vienna, A‐1090 Vienna, Austria</mods:affiliation></affiliation><affiliation><mods:affiliation>Correspondence address: Corresponding Author: Prof. Dr. Hans Lassmann, Institute of Neurology, University of Vienna, Schwarzspanierstrasse 17, A‐1090 Vienna; Tel.: (431) 427796–11; Fax: (431) 4277 97 96</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Brain Pathology</title><title level="j" type="alt">BRAIN PATHOLOGY</title><idno type="ISSN">1015-6305</idno><idno type="eISSN">1750-3639</idno><imprint><biblScope unit="vol">8</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="681">681</biblScope><biblScope unit="page" to="694">694</biblScope><biblScope unit="page-count">14</biblScope><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="1998-10">1998-10</date></imprint><idno type="ISSN">1015-6305</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1015-6305</idno></seriesStmt></fileDesc><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></keywords></textClass></profileDesc></teiHeader><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></TEI><istex><corpusName>wiley</corpusName><keywords><teeft><json:string>demyelination</json:string><json:string>myelin</json:string><json:string>optic</json:string><json:string>spinal</json:string><json:string>glycoprotein</json:string><json:string>oligodendrocyte</json:string><json:string>multiple sclerosis</json:string><json:string>demyelinating</json:string><json:string>encephalomyelitis</json:string><json:string>spinal cord</json:string><json:string>myelin oligodendrocyte glycoprotein</json:string><json:string>optica</json:string><json:string>neuromyelitis</json:string><json:string>sclerosis</json:string><json:string>storch</json:string><json:string>autoimmunity</json:string><json:string>sensitization</json:string><json:string>lassmann</json:string><json:string>neuromyelitis optica</json:string><json:string>neurol</json:string><json:string>granulocyte</json:string><json:string>cerebellar</json:string><json:string>lesional</json:string><json:string>luxol</json:string><json:string>optic nerves</json:string><json:string>lesion</json:string><json:string>periventricular</json:string><json:string>autoimmune</json:string><json:string>blue myelin stain</json:string><json:string>autoimmune encephalomyelitis</json:string><json:string>optic neuritis</json:string><json:string>macrophage</json:string><json:string>axon</json:string><json:string>myelitis</json:string><json:string>immunocytochemistry</json:string><json:string>demyelinated</json:string><json:string>inflammation</json:string><json:string>optic nerve</json:string><json:string>plaque</json:string><json:string>neuropathology</json:string><json:string>inflammatory</json:string><json:string>bielschowsky silver impregnation</json:string><json:string>present study</json:string><json:string>general neuropathology</json:string><json:string>neuritis</json:string><json:string>subpial demyelination</json:string><json:string>plaque distribution</json:string><json:string>environmental factors</json:string><json:string>active demyelination</json:string><json:string>demyelinating areas</json:string><json:string>chronic myelin oligodendrocyte glycoprotein</json:string><json:string>optic system</json:string><json:string>allergic encephalomyelitis</json:string><json:string>demyelinating lesions</json:string><json:string>lesional distribution</json:string><json:string>destructive lesions</json:string><json:string>cerebellar type</json:string><json:string>degenerating myelin sheaths</json:string><json:string>periventricular type</json:string><json:string>proteolipid protein</json:string><json:string>different markers</json:string><json:string>clinical neurology</json:string><json:string>demyelinating diseases</json:string><json:string>glial fibrillary acidic protein</json:string><json:string>significant differences</json:string><json:string>optic nerve involvement</json:string><json:string>genetic background</json:string><json:string>immune reactions</json:string><json:string>demyelinating antibodies</json:string><json:string>eosinophilic granulocytes</json:string><json:string>spinal type</json:string><json:string>rat</json:string></teeft></keywords><author><json:item><name>Maria K. Storch</name><affiliations><json:string>Neurological Institute, University of Vienna, A‐1090 Vienna, Austria</json:string></affiliations></json:item><json:item><name>Andreas Stefferl</name><affiliations><json:string>Max‐Planck‐Insitute for Neurobiology, D‐82152 Martinsried, Germany</json:string></affiliations></json:item><json:item><name>Uschi Brehm</name><affiliations><json:string>Max‐Planck‐Insitute for Neurobiology, D‐82152 Martinsried, Germany</json:string></affiliations></json:item><json:item><name>Robert Weissert</name><affiliations><json:string>Neuroimmunology Unit, Center of Molecular Medicine, Karolinska Hospital, S‐17176 Stockholm, Sweden</json:string></affiliations></json:item><json:item><name>Erik Wallström</name><affiliations><json:string>Neuroimmunology Unit, Center of Molecular Medicine, Karolinska Hospital, S‐17176 Stockholm, Sweden</json:string></affiliations></json:item><json:item><name>Martin Kerschensteiner</name><affiliations><json:string>Max‐Planck‐Insitute for Neurobiology, D‐82152 Martinsried, Germany</json:string></affiliations></json:item><json:item><name>Tomas Olsson</name><affiliations><json:string>Neuroimmunology Unit, Center of Molecular Medicine, Karolinska Hospital, S‐17176 Stockholm, Sweden</json:string></affiliations></json:item><json:item><name>Chris Linington</name><affiliations><json:string>Max‐Planck‐Insitute for Neurobiology, D‐82152 Martinsried, Germany</json:string></affiliations></json:item><json:item><name>Hans Lassmann</name><affiliations><json:string>Neurological Institute, University of Vienna, A‐1090 Vienna, Austria</json:string><json:string>Correspondence address: Corresponding Author: Prof. Dr. Hans Lassmann, Institute of Neurology, University of Vienna, Schwarzspanierstrasse 17, A‐1090 Vienna; Tel.: (431) 427796–11; Fax: (431) 4277 97 96</json:string></affiliations></json:item></author><articleId><json:string>BPA681</json:string></articleId><arkIstex>ark:/67375/WNG-FWL8W1CK-Z</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><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.</abstract><qualityIndicators><score>9.196</score><pdfWordCount>5457</pdfWordCount><pdfCharCount>37233</pdfCharCount><pdfVersion>1.2</pdfVersion><pdfPageCount>14</pdfPageCount><pdfPageSize>612 x 792 pts (letter)</pdfPageSize><pdfWordsPerPage>390</pdfWordsPerPage><pdfText>true</pdfText><refBibsNative>true</refBibsNative><abstractWordCount>183</abstractWordCount><abstractCharCount>1334</abstractCharCount><keywordCount>0</keywordCount></qualityIndicators><title>Autoimmunity to Myelin Oligodendrocyte Glycoprotein in Rats Mimics the Spectrum of Multiple Sclerosis Pathology</title><pmid><json:string>9804377</json:string></pmid><genre><json:string>article</json:string></genre><host><title>Brain Pathology</title><language><json:string>unknown</json:string></language><doi><json:string>10.1111/(ISSN)1750-3639</json:string></doi><issn><json:string>1015-6305</json:string></issn><eissn><json:string>1750-3639</json:string></eissn><publisherId><json:string>BPA</json:string></publisherId><volume>8</volume><issue>4</issue><pages><first>681</first><last>694</last><total>14</total></pages><genre><json:string>journal</json:string></genre></host><namedEntities><unitex><date><json:string>1998</json:string></date><geogName></geogName><orgName><json:string>Germany Neuroimmunology Unit, Center of Molecular Medicine, Karolinska Hospital</json:string><json:string>Austria Max-Planck-Insitute for Neurobiology</json:string><json:string>Affinity Research Products, Ilkeston, UK</json:string><json:string>State Serum Institute, Denmark</json:string><json:string>Austrian Science Research Fund</json:string><json:string>Neurological Institute, University of Vienna</json:string><json:string>Institute of Neurology, University of Vienna, Schwarzspanierstrasse</json:string><json:string>Sweden Multiple</json:string></orgName><orgName_funder></orgName_funder><orgName_provider></orgName_provider><persName><json:string>P. 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Storch et al</json:string></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/WNG-FWL8W1CK-Z</json:string></ark><categories><wos><json:string>1 - science</json:string><json:string>2 - pathology</json:string><json:string>2 - neurosciences</json:string><json:string>2 - clinical neurology</json:string></wos><scienceMetrix><json:string>1 - health sciences</json:string><json:string>2 - clinical medicine</json:string><json:string>3 - neurology & neurosurgery</json:string></scienceMetrix><scopus><json:string>1 - Health Sciences</json:string><json:string>2 - Medicine</json:string><json:string>3 - Clinical Neurology</json:string><json:string>1 - Health Sciences</json:string><json:string>2 - Medicine</json:string><json:string>3 - Pathology and Forensic Medicine</json:string><json:string>1 - Life Sciences</json:string><json:string>2 - Neuroscience</json:string><json:string>3 - General Neuroscience</json:string></scopus><inist><json:string>1 - sciences appliquees, 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Pathology</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="1998-10"></date></publicationStmt><notesStmt><note type="content-type" subtype="article" source="article" scheme="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</note><note type="publication-type" subtype="journal" scheme="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</note></notesStmt><sourceDesc><biblStruct type="article"><analytic><title level="a" type="main">Autoimmunity to Myelin Oligodendrocyte Glycoprotein in Rats Mimics the Spectrum of Multiple Sclerosis Pathology</title><author xml:id="author-0000"><persName><forename type="first">Maria K.</forename><surname>Storch</surname></persName><affiliation><orgName type="institution">Neurological Institute</orgName><orgName type="institution">University of Vienna</orgName><address><addrLine>A‐1090 Vienna</addrLine><addrLine>Austria</addrLine><country key="AT" xml:lang="en">AUSTRIA</country></address></affiliation></author><author xml:id="author-0001"><persName><forename type="first">Andreas</forename><surname>Stefferl</surname></persName><affiliation><orgName type="department">Max‐Planck‐Insitute for Neurobiology</orgName><address><addrLine>D‐82152 Martinsried</addrLine><addrLine>Germany</addrLine><country key="DE" xml:lang="en">GERMANY</country></address></affiliation></author><author xml:id="author-0002"><persName><forename type="first">Uschi</forename><surname>Brehm</surname></persName><affiliation><orgName type="department">Max‐Planck‐Insitute for Neurobiology</orgName><address><addrLine>D‐82152 Martinsried</addrLine><addrLine>Germany</addrLine><country key="DE" xml:lang="en">GERMANY</country></address></affiliation></author><author xml:id="author-0003"><persName><forename type="first">Robert</forename><surname>Weissert</surname></persName><affiliation><orgName type="laboratory">Neuroimmunology Unit</orgName><orgName type="institution">Center of Molecular Medicine</orgName><orgName type="institution">Karolinska Hospital</orgName><address><addrLine>S‐17176 Stockholm</addrLine><addrLine>Sweden</addrLine><country key="SE" xml:lang="en">SWEDEN</country></address></affiliation></author><author xml:id="author-0004"><persName><forename type="first">Erik</forename><surname>Wallström</surname></persName><affiliation><orgName type="laboratory">Neuroimmunology Unit</orgName><orgName type="institution">Center of Molecular Medicine</orgName><orgName type="institution">Karolinska Hospital</orgName><address><addrLine>S‐17176 Stockholm</addrLine><addrLine>Sweden</addrLine><country key="SE" xml:lang="en">SWEDEN</country></address></affiliation></author><author xml:id="author-0005"><persName><forename type="first">Martin</forename><surname>Kerschensteiner</surname></persName><affiliation><orgName type="department">Max‐Planck‐Insitute for Neurobiology</orgName><address><addrLine>D‐82152 Martinsried</addrLine><addrLine>Germany</addrLine><country key="DE" xml:lang="en">GERMANY</country></address></affiliation></author><author xml:id="author-0006"><persName><forename type="first">Tomas</forename><surname>Olsson</surname></persName><affiliation><orgName type="laboratory">Neuroimmunology Unit</orgName><orgName type="institution">Center of Molecular Medicine</orgName><orgName type="institution">Karolinska Hospital</orgName><address><addrLine>S‐17176 Stockholm</addrLine><addrLine>Sweden</addrLine><country key="SE" xml:lang="en">SWEDEN</country></address></affiliation></author><author xml:id="author-0007"><persName><forename type="first">Chris</forename><surname>Linington</surname></persName><affiliation><orgName type="department">Max‐Planck‐Insitute for Neurobiology</orgName><address><addrLine>D‐82152 Martinsried</addrLine><addrLine>Germany</addrLine><country key="DE" xml:lang="en">GERMANY</country></address></affiliation></author><author xml:id="author-0008" role="corresp"><persName><forename type="first">Hans</forename><surname>Lassmann</surname></persName><affiliation><orgName type="institution">Neurological Institute</orgName><orgName type="institution">University of Vienna</orgName><address><addrLine>A‐1090 Vienna</addrLine><addrLine>Austria</addrLine><country key="AT" xml:lang="en">AUSTRIA</country></address></affiliation></author><idno type="istex">289D82BFB5AAD1E0F90AD378A31CC4E77A71CBC7</idno><idno type="ark">ark:/67375/WNG-FWL8W1CK-Z</idno><idno type="DOI">10.1111/j.1750-3639.1998.tb00194.x</idno><idno type="unit">BPA681</idno><idno type="toTypesetVersion">file:BPA.BPA681.pdf</idno></analytic><monogr><title level="j" type="main">Brain Pathology</title><title level="j" type="alt">BRAIN PATHOLOGY</title><idno type="pISSN">1015-6305</idno><idno type="eISSN">1750-3639</idno><idno type="book-DOI">10.1111/(ISSN)1750-3639</idno><idno type="book-part-DOI">10.1111/bpa.1998.8.issue-4</idno><idno type="product">BPA</idno><idno type="publisherDivision">ST</idno><imprint><biblScope unit="vol">8</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="681">681</biblScope><biblScope unit="page" to="694">694</biblScope><biblScope unit="page-count">14</biblScope><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="1998-10"></date></imprint></monogr></biblStruct></sourceDesc></fileDesc><encodingDesc><schemaRef type="ODD" url="https://xml-schema.delivery.istex.fr/tei-istex.odd"></schemaRef><appInfo><application ident="pub2tei" version="1.0.10" when="2019-12-20"><label>pub2TEI-ISTEX</label><desc>A set of style sheets for converting XML documents encoded in various scientific publisher formats into a common TEI format.
<ref target="http://www.tei-c.org/">We use TEI</ref></desc></application></appInfo></encodingDesc><profileDesc><abstract xml:lang="en" style="main"><p>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.</p><p>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.</p></abstract><textClass><keywords rend="tocHeading1"><term>RESEARCH ARTICLE</term></keywords></textClass><langUsage><language ident="en"></language></langUsage></profileDesc><revisionDesc><change when="2019-12-20" who="#istex" xml:id="pub2tei">formatting</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/WNG-FWL8W1CK-Z/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Blackwell Publishing Ltd</publisherName><publisherLoc>Oxford, UK</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1750-3639</doi><issn type="print">1015-6305</issn><issn type="electronic">1750-3639</issn><idGroup><id type="product" value="BPA"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="BRAIN PATHOLOGY">Brain Pathology</title></titleGroup></publicationMeta><publicationMeta level="part" position="10104"><doi origin="wiley">10.1111/bpa.1998.8.issue-4</doi><numberingGroup><numbering type="journalVolume" number="8">8</numbering><numbering type="journalIssue" number="4">4</numbering></numberingGroup><coverDate startDate="1998-10">October 1998</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="0068100" status="forIssue"><doi origin="wiley">10.1111/j.1750-3639.1998.tb00194.x</doi><idGroup><id type="unit" value="BPA681"></id></idGroup><countGroup><count type="pageTotal" number="14"></count></countGroup><titleGroup><title type="tocHeading1">RESEARCH ARTICLE</title></titleGroup><eventGroup><event type="firstOnline" date="2006-04-05"></event><event type="publishedOnlineFinalForm" date="2006-04-05"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:3.3.2 mode:FullText" date="2014-06-12"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.3.2 mode:FullText" date="2014-06-12"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-15"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="681">681</numbering><numbering type="pageLast" number="694">694</numbering></numberingGroup><correspondenceTo>Corresponding Author: Prof. Dr. Hans Lassmann, Institute of Neurology, University of Vienna, Schwarzspanierstrasse 17, A‐1090 Vienna; Tel.: (431) 427796–11; Fax: (431) 4277 97 96</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:BPA.BPA681.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="referenceTotal" number="44"></count><count type="linksCrossRef" number="10"></count></countGroup><titleGroup><title type="main">Autoimmunity to Myelin Oligodendrocyte Glycoprotein in Rats Mimics the Spectrum of Multiple Sclerosis Pathology</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1"><personName><givenNames>Maria K.</givenNames><familyName>Storch</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a2"><personName><givenNames>Andreas</givenNames><familyName>Stefferl</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a2"><personName><givenNames>Uschi</givenNames><familyName>Brehm</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a3"><personName><givenNames>Robert</givenNames><familyName>Weissert</familyName></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a3"><personName><givenNames>Erik</givenNames><familyName>Wallström</familyName></personName></creator><creator creatorRole="author" xml:id="cr6" affiliationRef="#a2"><personName><givenNames>Martin</givenNames><familyName>Kerschensteiner</familyName></personName></creator><creator creatorRole="author" xml:id="cr7" affiliationRef="#a3"><personName><givenNames>Tomas</givenNames><familyName>Olsson</familyName></personName></creator><creator creatorRole="author" xml:id="cr8" affiliationRef="#a2"><personName><givenNames>Chris</givenNames><familyName>Linington</familyName></personName></creator><creator creatorRole="author" xml:id="cr9" affiliationRef="#a1" corresponding="yes"><personName><givenNames>Hans</givenNames><familyName>Lassmann</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="AT"><unparsedAffiliation>Neurological Institute, University of Vienna, A‐1090 Vienna, Austria</unparsedAffiliation></affiliation><affiliation xml:id="a2" countryCode="DE"><unparsedAffiliation>Max‐Planck‐Insitute for Neurobiology, D‐82152 Martinsried, Germany</unparsedAffiliation></affiliation><affiliation xml:id="a3" countryCode="SE"><unparsedAffiliation>Neuroimmunology Unit, Center of Molecular Medicine, Karolinska Hospital, S‐17176 Stockholm, Sweden</unparsedAffiliation></affiliation></affiliationGroup><abstractGroup><abstract type="main" xml:lang="en"><p>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.</p><p>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.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Autoimmunity to Myelin Oligodendrocyte Glycoprotein in Rats Mimics the Spectrum of Multiple Sclerosis Pathology</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Autoimmunity to Myelin Oligodendrocyte Glycoprotein in Rats Mimics the Spectrum of Multiple Sclerosis Pathology</title></titleInfo><name type="personal"><namePart type="given">Maria K.</namePart><namePart type="family">Storch</namePart><affiliation>Neurological Institute, University of Vienna, A‐1090 Vienna, Austria</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Andreas</namePart><namePart type="family">Stefferl</namePart><affiliation>Max‐Planck‐Insitute for Neurobiology, D‐82152 Martinsried, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Uschi</namePart><namePart type="family">Brehm</namePart><affiliation>Max‐Planck‐Insitute for Neurobiology, D‐82152 Martinsried, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Robert</namePart><namePart type="family">Weissert</namePart><affiliation>Neuroimmunology Unit, Center of Molecular Medicine, Karolinska Hospital, S‐17176 Stockholm, Sweden</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Erik</namePart><namePart type="family">Wallström</namePart><affiliation>Neuroimmunology Unit, Center of Molecular Medicine, Karolinska Hospital, S‐17176 Stockholm, Sweden</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Martin</namePart><namePart type="family">Kerschensteiner</namePart><affiliation>Max‐Planck‐Insitute for Neurobiology, D‐82152 Martinsried, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Tomas</namePart><namePart type="family">Olsson</namePart><affiliation>Neuroimmunology Unit, Center of Molecular Medicine, Karolinska Hospital, S‐17176 Stockholm, Sweden</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Chris</namePart><namePart type="family">Linington</namePart><affiliation>Max‐Planck‐Insitute for Neurobiology, D‐82152 Martinsried, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Hans</namePart><namePart type="family">Lassmann</namePart><affiliation>Neurological Institute, University of Vienna, A‐1090 Vienna, Austria</affiliation><affiliation>Correspondence address: Corresponding Author: Prof. Dr. Hans Lassmann, Institute of Neurology, University of Vienna, Schwarzspanierstrasse 17, A‐1090 Vienna; Tel.: (431) 427796–11; Fax: (431) 4277 97 96</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">1998-10</dateIssued><copyrightDate encoding="w3cdtf">1998</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><extent unit="references">44</extent><extent unit="linksCrossRef">10</extent></physicalDescription><abstract 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.</abstract><relatedItem type="host"><titleInfo><title>Brain Pathology</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><identifier type="ISSN">1015-6305</identifier><identifier type="eISSN">1750-3639</identifier><identifier type="DOI">10.1111/(ISSN)1750-3639</identifier><identifier type="PublisherID">BPA</identifier><part><date>1998</date><detail type="volume"><caption>vol.</caption><number>8</number></detail><detail type="issue"><caption>no.</caption><number>4</number></detail><extent unit="pages"><start>681</start><end>694</end><total>14</total></extent></part></relatedItem><relatedItem type="references" displayLabel="cit1"><titleInfo><title>The N‐terminal domain of the myelin oligodendrocyte glycoprotein (MOG) induces acute demyelinating experimental autoimmune encephalomyelitis in the Lewis rat</title></titleInfo><name type="personal"><namePart type="given">M</namePart><namePart type="family">Adelmann</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J</namePart><namePart type="family">Wood</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">I</namePart><namePart type="family">Benzel</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">P</namePart><namePart type="family">Fiori</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">H</namePart><namePart type="family">Lassmann</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">JM</namePart><namePart type="family">Matthieu</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">MV</namePart><namePart type="family">Gardinier</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">K</namePart><namePart type="family">Dornmair</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C</namePart><namePart type="family">Linington</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Adelmann M , Wood J , Benzel I , Fiori P , Lassmann H , Matthieu JM , Gardinier MV , Dornmair K , Linington C ( 1995 ) The N‐terminal domain of the myelin oligodendrocyte glycoprotein (MOG) induces acute demyelinating experimental autoimmune encephalomyelitis in the Lewis rat . 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