Polyclonal IgM and IgA block in vitro complement deposition mediated by anti-ganglioside antibodies in autoimmune neuropathies
Intravenous immunoglobulin (IVIG), consisting of IgG, is the first-line treatment for Guillain–Barré syndrome and multifocal motor neuropathy. IgG, but neither IgM nor IgA, has been demonstrated in vitro to inhibit complement deposition mediated by anti-ganglioside autoantibodies in sera from patien...
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| Veröffentlicht in: | International immunopharmacology 2016-11, Vol.40, p.11-15 |
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| creator | Sudo, Makoto Miyaji, Kazuki Späth, Peter J. Morita-Matsumoto, Kana Yamaguchi, Yoshiki Yuki, Nobuhiro |
| description | Intravenous immunoglobulin (IVIG), consisting of IgG, is the first-line treatment for Guillain–Barré syndrome and multifocal motor neuropathy. IgG, but neither IgM nor IgA, has been demonstrated in vitro to inhibit complement deposition mediated by anti-ganglioside autoantibodies in sera from patients with both conditions. The objective of this study is to investigate the in vitro effectiveness of IgM and IgA in inhibiting complement deposition to ganglioside/anti-ganglioside antibody complexes. Serum samples were obtained from patients with multifocal motor neuropathy associated with anti-GM1 IgM antibodies, Guillain–Barré syndrome associated with anti-GM1 IgG antibodies and Miller Fisher syndrome associated with anti-GQ1b IgG antibodies. Inhibition of complement deposition using different immunoglobulin preparations was measured by enzyme-linked immunosorbent assay. IgM/A-enriched IVIG and immunoglobulin isotypes (polyclonal IgM and IgA) showed higher potential in inhibiting complement deposition than standard IVIG. Although the safety concerns about the use of IgM and IgA for an immunotherapy still remain, IgM and IgA may serve as an alternative immunotherapy in those anti-ganglioside antibody-mediated neuropathies.
•We studied the in vitro efficacy of IgM/IgA in inhibiting complement deposition.•IgM and IgA were more effective at inhibiting complement deposition than IVIG.•IgM/A-rich IVIG was more effective at inhibiting complement deposition than IVIG.•IgM and IgA serve as an alternative immunotherapy in GBS and MMN. |
| doi_str_mv | 10.1016/j.intimp.2016.08.019 |
| format | Article |
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•We studied the in vitro efficacy of IgM/IgA in inhibiting complement deposition.•IgM and IgA were more effective at inhibiting complement deposition than IVIG.•IgM/A-rich IVIG was more effective at inhibiting complement deposition than IVIG.•IgM and IgA serve as an alternative immunotherapy in GBS and MMN.</description><identifier>ISSN: 1567-5769</identifier><identifier>EISSN: 1878-1705</identifier><identifier>DOI: 10.1016/j.intimp.2016.08.019</identifier><identifier>PMID: 27567246</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Anti-ganglioside antibody ; Antibodies ; Antibodies, Anti-Idiotypic - blood ; Antibodies, Anti-Idiotypic - immunology ; Autoantibodies ; Complement ; Complement System Proteins - immunology ; Deposition ; Enzyme-linked immunosorbent assay ; Guillain-Barre Syndrome - blood ; Guillain-Barre Syndrome - immunology ; Guillain–Barré syndrome ; Humans ; Immunoglobulin A ; Immunoglobulin A - pharmacology ; Immunoglobulin G ; Immunoglobulin M ; Immunoglobulin M - pharmacology ; Immunoglobulins ; Immunoglobulins, Intravenous - pharmacology ; Immunotherapy ; In vitro methods and tests ; Intravenous administration ; Intravenous immunoglobulin ; Isotypes ; Miller-Fisher syndrome ; Motor task performance ; Multifocal motor neuropathy ; Patients ; Progressive motor neuropathy ; Studies</subject><ispartof>International immunopharmacology, 2016-11, Vol.40, p.11-15</ispartof><rights>2016 Elsevier B.V.</rights><rights>Copyright © 2016 Elsevier B.V. All rights reserved.</rights><rights>Copyright Elsevier BV Nov 2016</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c456t-32d1c096ad57a2033e0a8f652af41d6dc87cc8f256d10c4265d16ff0c629bf013</citedby><cites>FETCH-LOGICAL-c456t-32d1c096ad57a2033e0a8f652af41d6dc87cc8f256d10c4265d16ff0c629bf013</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.intimp.2016.08.019$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,777,781,3537,27905,27906,45976</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27567246$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sudo, Makoto</creatorcontrib><creatorcontrib>Miyaji, Kazuki</creatorcontrib><creatorcontrib>Späth, Peter J.</creatorcontrib><creatorcontrib>Morita-Matsumoto, Kana</creatorcontrib><creatorcontrib>Yamaguchi, Yoshiki</creatorcontrib><creatorcontrib>Yuki, Nobuhiro</creatorcontrib><title>Polyclonal IgM and IgA block in vitro complement deposition mediated by anti-ganglioside antibodies in autoimmune neuropathies</title><title>International immunopharmacology</title><addtitle>Int Immunopharmacol</addtitle><description>Intravenous immunoglobulin (IVIG), consisting of IgG, is the first-line treatment for Guillain–Barré syndrome and multifocal motor neuropathy. IgG, but neither IgM nor IgA, has been demonstrated in vitro to inhibit complement deposition mediated by anti-ganglioside autoantibodies in sera from patients with both conditions. The objective of this study is to investigate the in vitro effectiveness of IgM and IgA in inhibiting complement deposition to ganglioside/anti-ganglioside antibody complexes. Serum samples were obtained from patients with multifocal motor neuropathy associated with anti-GM1 IgM antibodies, Guillain–Barré syndrome associated with anti-GM1 IgG antibodies and Miller Fisher syndrome associated with anti-GQ1b IgG antibodies. Inhibition of complement deposition using different immunoglobulin preparations was measured by enzyme-linked immunosorbent assay. IgM/A-enriched IVIG and immunoglobulin isotypes (polyclonal IgM and IgA) showed higher potential in inhibiting complement deposition than standard IVIG. Although the safety concerns about the use of IgM and IgA for an immunotherapy still remain, IgM and IgA may serve as an alternative immunotherapy in those anti-ganglioside antibody-mediated neuropathies.
•We studied the in vitro efficacy of IgM/IgA in inhibiting complement deposition.•IgM and IgA were more effective at inhibiting complement deposition than IVIG.•IgM/A-rich IVIG was more effective at inhibiting complement deposition than IVIG.•IgM and IgA serve as an alternative immunotherapy in GBS and MMN.</description><subject>Anti-ganglioside antibody</subject><subject>Antibodies</subject><subject>Antibodies, Anti-Idiotypic - blood</subject><subject>Antibodies, Anti-Idiotypic - immunology</subject><subject>Autoantibodies</subject><subject>Complement</subject><subject>Complement System Proteins - immunology</subject><subject>Deposition</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Guillain-Barre Syndrome - blood</subject><subject>Guillain-Barre Syndrome - immunology</subject><subject>Guillain–Barré syndrome</subject><subject>Humans</subject><subject>Immunoglobulin A</subject><subject>Immunoglobulin A - pharmacology</subject><subject>Immunoglobulin G</subject><subject>Immunoglobulin M</subject><subject>Immunoglobulin M - pharmacology</subject><subject>Immunoglobulins</subject><subject>Immunoglobulins, Intravenous - pharmacology</subject><subject>Immunotherapy</subject><subject>In vitro methods and tests</subject><subject>Intravenous administration</subject><subject>Intravenous immunoglobulin</subject><subject>Isotypes</subject><subject>Miller-Fisher syndrome</subject><subject>Motor task performance</subject><subject>Multifocal motor neuropathy</subject><subject>Patients</subject><subject>Progressive motor neuropathy</subject><subject>Studies</subject><issn>1567-5769</issn><issn>1878-1705</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kU-PFCEQxYnRuH_0GxhD4sVLt0B3A30x2WzU3WSNHvRMaKgeGWlogd5kLn52GWf14MFTQdWvXiXvIfSCkpYSyt_sWxeKW9aW1V9LZEvo-AidUylkQwUZHtf3wEUzCD6eoYuc94TUfk-fojMm6oT1_Bz9_Bz9wfgYtMe3u49YB1vrFZ58NN-xC_jelRSxicvqYYFQsIU1ZldcDHgB63QBi6dDXSyu2emw866OLfxuTNE6yEcZvZXolmULgANsKa66fKujZ-jJrH2G5w_1En19_-7L9U1z9-nD7fXVXWP6gZemY5YaMnJtB6EZ6TogWs58YHruqeXWSGGMnNnALSWmZ3ywlM8zMZyN00xod4len3TXFH9skItaXDbgvQ4Qt6yo7ARhPZWsoq_-QfdxS9WfSo0d63hPBK9Uf6JMijknmNWa3KLTQVGijvmovTrlo475KCJVzaeuvXwQ36bq3t-lP4FU4O0JgOrGvYOksnEQTHU6gSnKRvf_C78AQwak1Q</recordid><startdate>201611</startdate><enddate>201611</enddate><creator>Sudo, Makoto</creator><creator>Miyaji, Kazuki</creator><creator>Späth, Peter J.</creator><creator>Morita-Matsumoto, Kana</creator><creator>Yamaguchi, Yoshiki</creator><creator>Yuki, Nobuhiro</creator><general>Elsevier B.V</general><general>Elsevier BV</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>7QO</scope><scope>7T5</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>201611</creationdate><title>Polyclonal IgM and IgA block in vitro complement deposition mediated by anti-ganglioside antibodies in autoimmune neuropathies</title><author>Sudo, Makoto ; Miyaji, Kazuki ; Späth, Peter J. ; Morita-Matsumoto, Kana ; Yamaguchi, Yoshiki ; Yuki, Nobuhiro</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c456t-32d1c096ad57a2033e0a8f652af41d6dc87cc8f256d10c4265d16ff0c629bf013</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Anti-ganglioside antibody</topic><topic>Antibodies</topic><topic>Antibodies, Anti-Idiotypic - blood</topic><topic>Antibodies, Anti-Idiotypic - immunology</topic><topic>Autoantibodies</topic><topic>Complement</topic><topic>Complement System Proteins - immunology</topic><topic>Deposition</topic><topic>Enzyme-linked immunosorbent assay</topic><topic>Guillain-Barre Syndrome - blood</topic><topic>Guillain-Barre Syndrome - immunology</topic><topic>Guillain–Barré syndrome</topic><topic>Humans</topic><topic>Immunoglobulin A</topic><topic>Immunoglobulin A - pharmacology</topic><topic>Immunoglobulin G</topic><topic>Immunoglobulin M</topic><topic>Immunoglobulin M - pharmacology</topic><topic>Immunoglobulins</topic><topic>Immunoglobulins, Intravenous - pharmacology</topic><topic>Immunotherapy</topic><topic>In vitro methods and tests</topic><topic>Intravenous administration</topic><topic>Intravenous immunoglobulin</topic><topic>Isotypes</topic><topic>Miller-Fisher syndrome</topic><topic>Motor task performance</topic><topic>Multifocal motor neuropathy</topic><topic>Patients</topic><topic>Progressive motor neuropathy</topic><topic>Studies</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sudo, Makoto</creatorcontrib><creatorcontrib>Miyaji, Kazuki</creatorcontrib><creatorcontrib>Späth, Peter J.</creatorcontrib><creatorcontrib>Morita-Matsumoto, Kana</creatorcontrib><creatorcontrib>Yamaguchi, Yoshiki</creatorcontrib><creatorcontrib>Yuki, Nobuhiro</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Immunology Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>International immunopharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sudo, Makoto</au><au>Miyaji, Kazuki</au><au>Späth, Peter J.</au><au>Morita-Matsumoto, Kana</au><au>Yamaguchi, Yoshiki</au><au>Yuki, Nobuhiro</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Polyclonal IgM and IgA block in vitro complement deposition mediated by anti-ganglioside antibodies in autoimmune neuropathies</atitle><jtitle>International immunopharmacology</jtitle><addtitle>Int Immunopharmacol</addtitle><date>2016-11</date><risdate>2016</risdate><volume>40</volume><spage>11</spage><epage>15</epage><pages>11-15</pages><issn>1567-5769</issn><eissn>1878-1705</eissn><abstract>Intravenous immunoglobulin (IVIG), consisting of IgG, is the first-line treatment for Guillain–Barré syndrome and multifocal motor neuropathy. IgG, but neither IgM nor IgA, has been demonstrated in vitro to inhibit complement deposition mediated by anti-ganglioside autoantibodies in sera from patients with both conditions. The objective of this study is to investigate the in vitro effectiveness of IgM and IgA in inhibiting complement deposition to ganglioside/anti-ganglioside antibody complexes. Serum samples were obtained from patients with multifocal motor neuropathy associated with anti-GM1 IgM antibodies, Guillain–Barré syndrome associated with anti-GM1 IgG antibodies and Miller Fisher syndrome associated with anti-GQ1b IgG antibodies. Inhibition of complement deposition using different immunoglobulin preparations was measured by enzyme-linked immunosorbent assay. IgM/A-enriched IVIG and immunoglobulin isotypes (polyclonal IgM and IgA) showed higher potential in inhibiting complement deposition than standard IVIG. Although the safety concerns about the use of IgM and IgA for an immunotherapy still remain, IgM and IgA may serve as an alternative immunotherapy in those anti-ganglioside antibody-mediated neuropathies.
•We studied the in vitro efficacy of IgM/IgA in inhibiting complement deposition.•IgM and IgA were more effective at inhibiting complement deposition than IVIG.•IgM/A-rich IVIG was more effective at inhibiting complement deposition than IVIG.•IgM and IgA serve as an alternative immunotherapy in GBS and MMN.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>27567246</pmid><doi>10.1016/j.intimp.2016.08.019</doi><tpages>5</tpages></addata></record> |
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| subjects | Anti-ganglioside antibody Antibodies Antibodies, Anti-Idiotypic - blood Antibodies, Anti-Idiotypic - immunology Autoantibodies Complement Complement System Proteins - immunology Deposition Enzyme-linked immunosorbent assay Guillain-Barre Syndrome - blood Guillain-Barre Syndrome - immunology Guillain–Barré syndrome Humans Immunoglobulin A Immunoglobulin A - pharmacology Immunoglobulin G Immunoglobulin M Immunoglobulin M - pharmacology Immunoglobulins Immunoglobulins, Intravenous - pharmacology Immunotherapy In vitro methods and tests Intravenous administration Intravenous immunoglobulin Isotypes Miller-Fisher syndrome Motor task performance Multifocal motor neuropathy Patients Progressive motor neuropathy Studies |
| title | Polyclonal IgM and IgA block in vitro complement deposition mediated by anti-ganglioside antibodies in autoimmune neuropathies |
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