The extracellular domain of myelin oligodendrocyte glycoprotein elicits atypical experimental autoimmune encephalomyelitis in rat and Macaque species
Atypical models of experimental autoimmune encephalomyelitis (EAE) are advantageous in that the heterogeneity of clinical signs appears more reflective of those in multiple sclerosis (MS). Conversely, models of classical EAE feature stereotypic progression of an ascending flaccid paralysis that is n...
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| description | Atypical models of experimental autoimmune encephalomyelitis (EAE) are advantageous in that the heterogeneity of clinical signs appears more reflective of those in multiple sclerosis (MS). Conversely, models of classical EAE feature stereotypic progression of an ascending flaccid paralysis that is not a characteristic of MS. The study of atypical EAE however has been limited due to the relative lack of suitable models that feature reliable disease incidence and severity, excepting mice deficient in gamma-interferon signaling pathways. In this study, atypical EAE was induced in Lewis rats, and a related approach was effective for induction of an unusual neurologic syndrome in a cynomolgus macaque. Lewis rats were immunized with the rat immunoglobulin variable (IgV)-related extracellular domain of myelin oligodendrocyte glycoprotein (IgV-MOG) in complete Freund's adjuvant (CFA) followed by one or more injections of rat IgV-MOG in incomplete Freund's adjuvant (IFA). The resulting disease was marked by torticollis, unilateral rigid paralysis, forelimb weakness, and high titers of anti-MOG antibody against conformational epitopes of MOG, as well as other signs of atypical EAE. A similar strategy elicited a distinct atypical form of EAE in a cynomolgus macaque. By day 36 in the monkey, titers of IgG against conformational epitopes of extracellular MOG were evident, and on day 201, the macaque had an abrupt onset of an unusual form of EAE that included a pronounced arousal-dependent, transient myotonia. The disease persisted for 6-7 weeks and was marked by a gradual, consistent improvement and an eventual full recovery without recurrence. These data indicate that one or more boosters of IgV-MOG in IFA represent a key variable for induction of atypical or unusual forms of EAE in rat and Macaca species. These studies also reveal a close correlation between humoral immunity against conformational epitopes of MOG, extended confluent demyelinating plaques in spinal cord and brainstem, and atypical disease induction. |
| doi_str_mv | 10.1371/journal.pone.0110048 |
| format | Article |
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Conversely, models of classical EAE feature stereotypic progression of an ascending flaccid paralysis that is not a characteristic of MS. The study of atypical EAE however has been limited due to the relative lack of suitable models that feature reliable disease incidence and severity, excepting mice deficient in gamma-interferon signaling pathways. In this study, atypical EAE was induced in Lewis rats, and a related approach was effective for induction of an unusual neurologic syndrome in a cynomolgus macaque. Lewis rats were immunized with the rat immunoglobulin variable (IgV)-related extracellular domain of myelin oligodendrocyte glycoprotein (IgV-MOG) in complete Freund's adjuvant (CFA) followed by one or more injections of rat IgV-MOG in incomplete Freund's adjuvant (IFA). The resulting disease was marked by torticollis, unilateral rigid paralysis, forelimb weakness, and high titers of anti-MOG antibody against conformational epitopes of MOG, as well as other signs of atypical EAE. A similar strategy elicited a distinct atypical form of EAE in a cynomolgus macaque. By day 36 in the monkey, titers of IgG against conformational epitopes of extracellular MOG were evident, and on day 201, the macaque had an abrupt onset of an unusual form of EAE that included a pronounced arousal-dependent, transient myotonia. The disease persisted for 6-7 weeks and was marked by a gradual, consistent improvement and an eventual full recovery without recurrence. These data indicate that one or more boosters of IgV-MOG in IFA represent a key variable for induction of atypical or unusual forms of EAE in rat and Macaca species. These studies also reveal a close correlation between humoral immunity against conformational epitopes of MOG, extended confluent demyelinating plaques in spinal cord and brainstem, and atypical disease induction.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0110048</identifier><identifier>PMID: 25303101</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Animal models ; Animals ; Antigenic determinants ; Antigens ; Arousal ; Biological response modifiers ; Biology and life sciences ; Brain research ; Brain stem ; Correlation analysis ; Data recovery ; Demyelination ; Encephalomyelitis ; Encephalomyelitis, Autoimmune, Experimental - immunology ; Epitopes ; Experimental allergic encephalomyelitis ; Female ; Freund's incomplete adjuvant ; Glycoproteins ; Humoral immunity ; Immunity ; Immunization ; Immunoglobulin G ; Immunoglobulin G - immunology ; Immunology ; Interferon ; Interferon-gamma - immunology ; Laboratories ; Localization ; Macaca fascicularis - immunology ; Male ; Medicine ; Medicine and Health Sciences ; Monkeys & apes ; Multiple sclerosis ; Myelin ; Myelin proteins ; Myelin-Oligodendrocyte Glycoprotein - immunology ; Myotonia ; Nervous system ; Nervous system diseases ; Oligodendrocyte-myelin glycoprotein ; Paralysis ; Peptides ; Physiology ; Plaques ; Proteins ; Rats ; Rats, Inbred Lew ; Research and Analysis Methods ; Rodents ; Signaling ; Spinal cord ; Torticollis ; γ-Interferon</subject><ispartof>PloS one, 2014-10, Vol.9 (10), p.e110048-e110048</ispartof><rights>COPYRIGHT 2014 Public Library of Science</rights><rights>2014 Curtis, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2014 Curtis, et al 2014 Curtis, et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-6d1f9a67c5e6f4455d7b1892c2c922ce1db2bfbf28b0acc6feecb0763c0757693</citedby><cites>FETCH-LOGICAL-c692t-6d1f9a67c5e6f4455d7b1892c2c922ce1db2bfbf28b0acc6feecb0763c0757693</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4193844/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4193844/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2095,2914,23846,27903,27904,53770,53772,79347,79348</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25303101$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>de Castro, Fernando</contributor><creatorcontrib>Curtis, 2nd, Alan D</creatorcontrib><creatorcontrib>Taslim, Najla</creatorcontrib><creatorcontrib>Reece, Shaun P</creatorcontrib><creatorcontrib>Grebenciucova, Elena</creatorcontrib><creatorcontrib>Ray, Richard H</creatorcontrib><creatorcontrib>Rosenbaum, Matthew D</creatorcontrib><creatorcontrib>Wardle, Robert L</creatorcontrib><creatorcontrib>Van Scott, Michael R</creatorcontrib><creatorcontrib>Mannie, Mark D</creatorcontrib><title>The extracellular domain of myelin oligodendrocyte glycoprotein elicits atypical experimental autoimmune encephalomyelitis in rat and Macaque species</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Atypical models of experimental autoimmune encephalomyelitis (EAE) are advantageous in that the heterogeneity of clinical signs appears more reflective of those in multiple sclerosis (MS). Conversely, models of classical EAE feature stereotypic progression of an ascending flaccid paralysis that is not a characteristic of MS. The study of atypical EAE however has been limited due to the relative lack of suitable models that feature reliable disease incidence and severity, excepting mice deficient in gamma-interferon signaling pathways. In this study, atypical EAE was induced in Lewis rats, and a related approach was effective for induction of an unusual neurologic syndrome in a cynomolgus macaque. Lewis rats were immunized with the rat immunoglobulin variable (IgV)-related extracellular domain of myelin oligodendrocyte glycoprotein (IgV-MOG) in complete Freund's adjuvant (CFA) followed by one or more injections of rat IgV-MOG in incomplete Freund's adjuvant (IFA). The resulting disease was marked by torticollis, unilateral rigid paralysis, forelimb weakness, and high titers of anti-MOG antibody against conformational epitopes of MOG, as well as other signs of atypical EAE. A similar strategy elicited a distinct atypical form of EAE in a cynomolgus macaque. By day 36 in the monkey, titers of IgG against conformational epitopes of extracellular MOG were evident, and on day 201, the macaque had an abrupt onset of an unusual form of EAE that included a pronounced arousal-dependent, transient myotonia. The disease persisted for 6-7 weeks and was marked by a gradual, consistent improvement and an eventual full recovery without recurrence. These data indicate that one or more boosters of IgV-MOG in IFA represent a key variable for induction of atypical or unusual forms of EAE in rat and Macaca species. These studies also reveal a close correlation between humoral immunity against conformational epitopes of MOG, extended confluent demyelinating plaques in spinal cord and brainstem, and atypical disease induction.</description><subject>Animal models</subject><subject>Animals</subject><subject>Antigenic determinants</subject><subject>Antigens</subject><subject>Arousal</subject><subject>Biological response modifiers</subject><subject>Biology and life sciences</subject><subject>Brain research</subject><subject>Brain stem</subject><subject>Correlation analysis</subject><subject>Data recovery</subject><subject>Demyelination</subject><subject>Encephalomyelitis</subject><subject>Encephalomyelitis, Autoimmune, Experimental - immunology</subject><subject>Epitopes</subject><subject>Experimental allergic encephalomyelitis</subject><subject>Female</subject><subject>Freund's incomplete adjuvant</subject><subject>Glycoproteins</subject><subject>Humoral 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L</au><au>Van Scott, Michael R</au><au>Mannie, Mark D</au><au>de Castro, Fernando</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The extracellular domain of myelin oligodendrocyte glycoprotein elicits atypical experimental autoimmune encephalomyelitis in rat and Macaque species</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2014-10-10</date><risdate>2014</risdate><volume>9</volume><issue>10</issue><spage>e110048</spage><epage>e110048</epage><pages>e110048-e110048</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Atypical models of experimental autoimmune encephalomyelitis (EAE) are advantageous in that the heterogeneity of clinical signs appears more reflective of those in multiple sclerosis (MS). Conversely, models of classical EAE feature stereotypic progression of an ascending flaccid paralysis that is not a characteristic of MS. The study of atypical EAE however has been limited due to the relative lack of suitable models that feature reliable disease incidence and severity, excepting mice deficient in gamma-interferon signaling pathways. In this study, atypical EAE was induced in Lewis rats, and a related approach was effective for induction of an unusual neurologic syndrome in a cynomolgus macaque. Lewis rats were immunized with the rat immunoglobulin variable (IgV)-related extracellular domain of myelin oligodendrocyte glycoprotein (IgV-MOG) in complete Freund's adjuvant (CFA) followed by one or more injections of rat IgV-MOG in incomplete Freund's adjuvant (IFA). The resulting disease was marked by torticollis, unilateral rigid paralysis, forelimb weakness, and high titers of anti-MOG antibody against conformational epitopes of MOG, as well as other signs of atypical EAE. A similar strategy elicited a distinct atypical form of EAE in a cynomolgus macaque. By day 36 in the monkey, titers of IgG against conformational epitopes of extracellular MOG were evident, and on day 201, the macaque had an abrupt onset of an unusual form of EAE that included a pronounced arousal-dependent, transient myotonia. The disease persisted for 6-7 weeks and was marked by a gradual, consistent improvement and an eventual full recovery without recurrence. These data indicate that one or more boosters of IgV-MOG in IFA represent a key variable for induction of atypical or unusual forms of EAE in rat and Macaca species. These studies also reveal a close correlation between humoral immunity against conformational epitopes of MOG, extended confluent demyelinating plaques in spinal cord and brainstem, and atypical disease induction.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>25303101</pmid><doi>10.1371/journal.pone.0110048</doi><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2014-10, Vol.9 (10), p.e110048-e110048 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1610133575 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS); EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Animal models Animals Antigenic determinants Antigens Arousal Biological response modifiers Biology and life sciences Brain research Brain stem Correlation analysis Data recovery Demyelination Encephalomyelitis Encephalomyelitis, Autoimmune, Experimental - immunology Epitopes Experimental allergic encephalomyelitis Female Freund's incomplete adjuvant Glycoproteins Humoral immunity Immunity Immunization Immunoglobulin G Immunoglobulin G - immunology Immunology Interferon Interferon-gamma - immunology Laboratories Localization Macaca fascicularis - immunology Male Medicine Medicine and Health Sciences Monkeys & apes Multiple sclerosis Myelin Myelin proteins Myelin-Oligodendrocyte Glycoprotein - immunology Myotonia Nervous system Nervous system diseases Oligodendrocyte-myelin glycoprotein Paralysis Peptides Physiology Plaques Proteins Rats Rats, Inbred Lew Research and Analysis Methods Rodents Signaling Spinal cord Torticollis γ-Interferon |
| title | The extracellular domain of myelin oligodendrocyte glycoprotein elicits atypical experimental autoimmune encephalomyelitis in rat and Macaque species |
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