Neuromyelitis optica MOG-IgG causes reversible lesions in mouse brain
Antibodies against myelin oligodendrocyte glycoprotein (MOG-IgG) are present in some neuromyelitis optica patients who lack antibodies against aquaporin-4 (AQP4-IgG). The effects of neuromyelitis optica MOG-IgG in the central nervous system have not been investigated in vivo. We microinjected MOG-Ig...
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| Veröffentlicht in: | Acta neuropathologica communications 2014-03, Vol.2 (1), p.35-35, Article 35 |
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| creator | Saadoun, Samira Waters, Patrick Owens, Gregory P Bennett, Jeffrey L Vincent, Angela Papadopoulos, Marios C |
| description | Antibodies against myelin oligodendrocyte glycoprotein (MOG-IgG) are present in some neuromyelitis optica patients who lack antibodies against aquaporin-4 (AQP4-IgG). The effects of neuromyelitis optica MOG-IgG in the central nervous system have not been investigated in vivo. We microinjected MOG-IgG, obtained from patients with neuromyelitis optica, into mouse brains and compared the results with AQP4-IgG.
MOG-IgG caused myelin changes and altered the expression of axonal proteins that are essential for action potential firing, but did not produce inflammation, axonal loss, neuronal or astrocyte death. These changes were independent of complement and recovered within two weeks. By contrast, AQP4-IgG produced complement-mediated myelin loss, neuronal and astrocyte death with limited recovery at two weeks.
These differences mirror the better outcomes for MOG-IgG compared with AQP4-IgG patients and raise the possibility that MOG-IgG contributes to pathology in some neuromyelitis optica patients. |
| doi_str_mv | 10.1186/2051-5960-2-35 |
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MOG-IgG caused myelin changes and altered the expression of axonal proteins that are essential for action potential firing, but did not produce inflammation, axonal loss, neuronal or astrocyte death. These changes were independent of complement and recovered within two weeks. By contrast, AQP4-IgG produced complement-mediated myelin loss, neuronal and astrocyte death with limited recovery at two weeks.
These differences mirror the better outcomes for MOG-IgG compared with AQP4-IgG patients and raise the possibility that MOG-IgG contributes to pathology in some neuromyelitis optica patients.</description><identifier>ISSN: 2051-5960</identifier><identifier>EISSN: 2051-5960</identifier><identifier>DOI: 10.1186/2051-5960-2-35</identifier><identifier>PMID: 24685353</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Animals ; Aquaporin 4 - immunology ; Astrocytes - drug effects ; Brain Injuries - chemically induced ; Brain Injuries - immunology ; Brain Injuries - pathology ; Cell Adhesion Molecules, Neuronal - metabolism ; Comparative analysis ; Humans ; Immunoglobulin G - toxicity ; Mice ; Myelin Basic Protein - metabolism ; Myelin-Oligodendrocyte Glycoprotein - immunology ; Nerve Tissue Proteins - metabolism ; Neuromyelitis Optica - immunology ; Neuromyelitis Optica - metabolism ; Neurons ; Neurons - drug effects ; Neurons - pathology ; Physiological aspects ; Sodium Channels - metabolism ; Time Factors</subject><ispartof>Acta neuropathologica communications, 2014-03, Vol.2 (1), p.35-35, Article 35</ispartof><rights>COPYRIGHT 2014 BioMed Central Ltd.</rights><rights>Copyright © 2014 Saadoun et al.; licensee BioMed Central Ltd. 2014 Saadoun et al.; licensee BioMed Central Ltd.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c488t-694632702b0124e91396fedc601fca46d7af9cc2c71b49ac32f4ff2b7c293af43</citedby><cites>FETCH-LOGICAL-c488t-694632702b0124e91396fedc601fca46d7af9cc2c71b49ac32f4ff2b7c293af43</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/PMC3977893/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3977893/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27903,27904,53769,53771</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24685353$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Saadoun, Samira</creatorcontrib><creatorcontrib>Waters, Patrick</creatorcontrib><creatorcontrib>Owens, Gregory P</creatorcontrib><creatorcontrib>Bennett, Jeffrey L</creatorcontrib><creatorcontrib>Vincent, Angela</creatorcontrib><creatorcontrib>Papadopoulos, Marios C</creatorcontrib><title>Neuromyelitis optica MOG-IgG causes reversible lesions in mouse brain</title><title>Acta neuropathologica communications</title><addtitle>Acta Neuropathol Commun</addtitle><description>Antibodies against myelin oligodendrocyte glycoprotein (MOG-IgG) are present in some neuromyelitis optica patients who lack antibodies against aquaporin-4 (AQP4-IgG). The effects of neuromyelitis optica MOG-IgG in the central nervous system have not been investigated in vivo. We microinjected MOG-IgG, obtained from patients with neuromyelitis optica, into mouse brains and compared the results with AQP4-IgG.
MOG-IgG caused myelin changes and altered the expression of axonal proteins that are essential for action potential firing, but did not produce inflammation, axonal loss, neuronal or astrocyte death. These changes were independent of complement and recovered within two weeks. By contrast, AQP4-IgG produced complement-mediated myelin loss, neuronal and astrocyte death with limited recovery at two weeks.
These differences mirror the better outcomes for MOG-IgG compared with AQP4-IgG patients and raise the possibility that MOG-IgG contributes to pathology in some neuromyelitis optica patients.</description><subject>Animals</subject><subject>Aquaporin 4 - immunology</subject><subject>Astrocytes - drug effects</subject><subject>Brain Injuries - chemically induced</subject><subject>Brain Injuries - immunology</subject><subject>Brain Injuries - pathology</subject><subject>Cell Adhesion Molecules, Neuronal - metabolism</subject><subject>Comparative analysis</subject><subject>Humans</subject><subject>Immunoglobulin G - toxicity</subject><subject>Mice</subject><subject>Myelin Basic Protein - metabolism</subject><subject>Myelin-Oligodendrocyte Glycoprotein - immunology</subject><subject>Nerve Tissue Proteins - metabolism</subject><subject>Neuromyelitis Optica - immunology</subject><subject>Neuromyelitis Optica - metabolism</subject><subject>Neurons</subject><subject>Neurons - drug effects</subject><subject>Neurons - pathology</subject><subject>Physiological aspects</subject><subject>Sodium Channels - metabolism</subject><subject>Time Factors</subject><issn>2051-5960</issn><issn>2051-5960</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNptkUtrAjEUhUNpqcW67bIECt2NzWse2RRErBVs3bTrkImJpsxMJBkF_30z2IqCySLh3nMON_kAeMBoiHGRvRCU4iTlGUpIQtMrcHcsXJ_ce2AQwg-Ki2NMi-IW9AjLipSm9A5MPvXWu3qvK9vaAN2mtUrCj8U0ma2mUMlt0AF6vdM-2LLSsNLBuiZA28DaxSYsvbTNPbgxsgp68Hf2wffb5Gv8nswX09l4NE8UK4o2yTjLKMkRKREmTHNMeWb0UmUIGyVZtsyl4UoRleOScakoMcwYUuaKcCoNo33wesjdbMs6GnXTelmJjbe19HvhpBXnncauxcrtBOV5XnAaA54OAStZaWEb46JM1TYoMUoZjrNhjKJqeEEV91LXVrlGGxvrZ4bnE8Nay6pdB1dt2-6vLiYr70Lw2hxnx0h0TEWHTXTYBBGRUB88nr74KP8nSH8Blt-aiw</recordid><startdate>20140331</startdate><enddate>20140331</enddate><creator>Saadoun, Samira</creator><creator>Waters, Patrick</creator><creator>Owens, Gregory P</creator><creator>Bennett, Jeffrey L</creator><creator>Vincent, Angela</creator><creator>Papadopoulos, Marios C</creator><general>BioMed Central Ltd</general><general>BioMed Central</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>5PM</scope></search><sort><creationdate>20140331</creationdate><title>Neuromyelitis optica MOG-IgG causes reversible lesions in mouse brain</title><author>Saadoun, Samira ; Waters, Patrick ; Owens, Gregory P ; Bennett, Jeffrey L ; Vincent, Angela ; Papadopoulos, Marios C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c488t-694632702b0124e91396fedc601fca46d7af9cc2c71b49ac32f4ff2b7c293af43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Animals</topic><topic>Aquaporin 4 - immunology</topic><topic>Astrocytes - drug effects</topic><topic>Brain Injuries - chemically induced</topic><topic>Brain Injuries - immunology</topic><topic>Brain Injuries - pathology</topic><topic>Cell Adhesion Molecules, Neuronal - metabolism</topic><topic>Comparative analysis</topic><topic>Humans</topic><topic>Immunoglobulin G - toxicity</topic><topic>Mice</topic><topic>Myelin Basic Protein - metabolism</topic><topic>Myelin-Oligodendrocyte Glycoprotein - immunology</topic><topic>Nerve Tissue Proteins - metabolism</topic><topic>Neuromyelitis Optica - immunology</topic><topic>Neuromyelitis Optica - metabolism</topic><topic>Neurons</topic><topic>Neurons - drug effects</topic><topic>Neurons - pathology</topic><topic>Physiological aspects</topic><topic>Sodium Channels - metabolism</topic><topic>Time Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Saadoun, Samira</creatorcontrib><creatorcontrib>Waters, Patrick</creatorcontrib><creatorcontrib>Owens, Gregory P</creatorcontrib><creatorcontrib>Bennett, Jeffrey L</creatorcontrib><creatorcontrib>Vincent, Angela</creatorcontrib><creatorcontrib>Papadopoulos, Marios C</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Acta neuropathologica communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Saadoun, Samira</au><au>Waters, Patrick</au><au>Owens, Gregory P</au><au>Bennett, Jeffrey L</au><au>Vincent, Angela</au><au>Papadopoulos, Marios C</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Neuromyelitis optica MOG-IgG causes reversible lesions in mouse brain</atitle><jtitle>Acta neuropathologica communications</jtitle><addtitle>Acta Neuropathol Commun</addtitle><date>2014-03-31</date><risdate>2014</risdate><volume>2</volume><issue>1</issue><spage>35</spage><epage>35</epage><pages>35-35</pages><artnum>35</artnum><issn>2051-5960</issn><eissn>2051-5960</eissn><abstract>Antibodies against myelin oligodendrocyte glycoprotein (MOG-IgG) are present in some neuromyelitis optica patients who lack antibodies against aquaporin-4 (AQP4-IgG). The effects of neuromyelitis optica MOG-IgG in the central nervous system have not been investigated in vivo. We microinjected MOG-IgG, obtained from patients with neuromyelitis optica, into mouse brains and compared the results with AQP4-IgG.
MOG-IgG caused myelin changes and altered the expression of axonal proteins that are essential for action potential firing, but did not produce inflammation, axonal loss, neuronal or astrocyte death. These changes were independent of complement and recovered within two weeks. By contrast, AQP4-IgG produced complement-mediated myelin loss, neuronal and astrocyte death with limited recovery at two weeks.
These differences mirror the better outcomes for MOG-IgG compared with AQP4-IgG patients and raise the possibility that MOG-IgG contributes to pathology in some neuromyelitis optica patients.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>24685353</pmid><doi>10.1186/2051-5960-2-35</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; DOAJ Directory of Open Access Journals; PubMed Central Open Access; Springer Nature OA Free Journals; Springer Nature - Complete Springer Journals; EZB-FREE-00999 freely available EZB journals; PubMed Central |
| subjects | Animals Aquaporin 4 - immunology Astrocytes - drug effects Brain Injuries - chemically induced Brain Injuries - immunology Brain Injuries - pathology Cell Adhesion Molecules, Neuronal - metabolism Comparative analysis Humans Immunoglobulin G - toxicity Mice Myelin Basic Protein - metabolism Myelin-Oligodendrocyte Glycoprotein - immunology Nerve Tissue Proteins - metabolism Neuromyelitis Optica - immunology Neuromyelitis Optica - metabolism Neurons Neurons - drug effects Neurons - pathology Physiological aspects Sodium Channels - metabolism Time Factors |
| title | Neuromyelitis optica MOG-IgG causes reversible lesions in mouse brain |
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