免疫関連性ニューロパチー (第49回日本神経学会総会(2008年) ; シンポジウム 末梢神経障害の研究--最近の進歩)
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- Material Type
- 記事
- Title
- Author/Editor
- 楠 進
- Series Title
- Author Heading
- Alternative Title
- Immune-mediated neuropathy
- Periodical title
- 臨床神経学 = Clinical neurology / 日本神経学会 編
- No. or year of volume/issue
- 48(11) 2008.11
- Volume
- 48
- Issue
- 11
- Pages
- 1023～1025
- Publication date of volume/issue (W3CDTF)
- 2008-11
- ISSN (Periodical Title)
- 0009-918X
- ISSN-L (Periodical Title)
- 0009-918X
- Publication (Periodical Title)
- 東京 : 日本神経学会
- Place of Publication (Country Code)
- JP
- Text Language Code
- jpn
- Subject Heading
- NDLC
- Target Audience
- 一般
- Holding library
- 国立国会図書館
- Call No.
- Z19-298
- Data Provider (Database)
- 国立国会図書館 : 国立国会図書館雑誌記事索引
- Bibliographic ID (NDL)
- 9758131
- Bibliographic Record Category (NDL)
- 632
- Summary, etc.
- Guillain-Barré syndrome (GBS) has two types; acute inflammatory demyelinating polyneuropathy (AIDP) and acute motor axonal neuropathy (AMAN). Recently, a nation-wide retrospective study showed that the rate of AMAN is higher in Japan than in western countries. A prospective study is now in progress. Elevated titers of serum anti-ganglioside antibodies are characteristic of GBS. Complement system has been shown to be involved in the anti-ganglioside antibody-mediated pathogenetic mechanisms. Some GBS patients have antibodies specific to a conformational epitope formed by two different gangliosides. Among such anti-ganglioside complex antibodies, anti-GD1a/GD1b IgG antibodies are shown to be associated with severe GBS requiring artificial ventilation. In contrast, antibodies highly specific to GD1b are associated with GBS with ataxia. Sensory ataxic neuropathy is induced by sensitization of rabbits with GD1b. An apoptotic mechanism has recently been shown to be involved in the pathogenesis of this animal model. Most of the patients with Fisher syndrome have anti-GQ1b IgG antibodies. Recent investigation on anti-ganglioside complex antibody showed that antibodies in Fisher syndrome can be subdivided into the three groups; GQ1b-specific, GQ1b/GM1-specific, and GQ1b/GD1a-specific. Research on antibodies to gangliosides and ganglioside complexes will provide us with a clue to develop a novel treatment of GBS.<br>
- DOI
- 10.5692/clinicalneurol.48.1023
- Access Restrictions
- インターネット公開
- Data Provider (Database)
- 科学技術振興機構 : J-STAGE
- Summary, etc.
- Guillain-Barré syndrome (GBS) has two types; acute inflammatory demyelinating polyneuropathy (AIDP) and acute motor axonal neuropathy (AMAN). Recently, a nation-wide retrospective study showed that the rate of AMAN is higher in Japan than in western countries. A prospective study is now in progress. Elevated titers of serum anti-ganglioside antibodies are characteristic of GBS. Complement system has been shown to be involved in the anti-ganglioside antibody-mediated pathogenetic mechanisms. Some GBS patients have antibodies specific to a conformational epitope formed by two different gangliosides. Among such anti-ganglioside complex antibodies, anti-GD1a/GD1b IgG antibodies are shown to be associated with severe GBS requiring artificial ventilation. In contrast, antibodies highly specific to GD1b are associated with GBS with ataxia. Sensory ataxic neuropathy is induced by sensitization of rabbits with GD1b. An apoptotic mechanism has recently been shown to be involved in the pathogenesis of this animal model. Most of the patients with Fisher syndrome have anti-GQ1b IgG antibodies. Recent investigation on anti-ganglioside complex antibody showed that antibodies in Fisher syndrome can be subdivided into the three groups; GQ1b-specific, GQ1b/GM1-specific, and GQ1b/GD1a-specific. Research on antibodies to gangliosides and ganglioside complexes will provide us with a clue to develop a novel treatment of GBS.<br>
- DOI
- 10.5692/clinicalneurol.48.1023
- Access Restrictions
- インターネット公開
- Related Material (URI)
- References
- Anti-ganglioside complex antibodies associated with severe disability in GBSGD1b-specific antibody induces ataxia in Guillain-Barré syndromeAnti-GM1 Antibodies Cause Complement-Mediated Disruption of Sodium Channel Clusters in Peripheral Motor Nerve FibersElectrophysiological classification of guillain‐barré syndrome: Clinical associations and outcomeApoptosis of primary sensory neurons in GD1b-induced sensory ataxic neuropathyEculizumab prevents anti-ganglioside antibody-mediated neuropathy in a murine modelAnti-ganglioside complex antibodies in Miller Fisher syndromeGanglioside complexes as new target antigens in Guillain–Barré syndromeAnti-ganglioside antibody-mediated neuronal cytotoxicity and its protection by intravenous immunoglobulin: implications for immune neuropathies
- Data Provider (Database)
- 国立情報学研究所 : CiNii Research
- Original Data Provider (Database)
- Japan Link Center雑誌記事索引データベースCrossrefCiNii Articles
- Bibliographic ID (NDL)
- 9758131
- NAID
- 10024898855