2022 Fiscal Year Final Research Report
Analysis of antibodies to glycolipid-protein complexes and elucidation of pathology in autoimmune-mediated demyelinating neuropathies
Project/Area Number |
20K07894
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Review Section |
Basic Section 52020:Neurology-related
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Research Institution | Kindai University |
Principal Investigator |
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Co-Investigator(Kenkyū-buntansha) |
楠 進 近畿大学, 医学部, 教授 (90195438)
宮本 勝一 近畿大学, 医学部, 准教授 (50388526)
山岸 裕子 近畿大学, 医学部, 講師 (80826040)
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Project Period (FY) |
2020-04-01 – 2023-03-31
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Keywords | 糖脂質 / 蛋白 / 自己抗体 / 脱髄性ニューロパチー / ギラン・バレー症候群 / 慢性炎症性脱髄性多発根ニューロパチー |
Outline of Final Research Achievements |
For elucidation of pathology in immune-mediated demyelinating neuropathies, we examined antibodies to glycolipid-protein complex which are consisting of one glycolipid (GM1 or GD1b) and one protein (NF155, CNTN1, or CASPR1) using ELISA. However, such antibody reactivities to glycolipid-protein complex were not observed in Guillain-Barre syndrome. Additionally, we examined Ca2+-dependent antibodies to paranodal proteins in patients who were suspected to be autoimmune nodopathies, whereas these were not detected. On the other hand, we clarified the presence of antibody reactivities to GQ1b in a few patients with chronic inflammatory demyelinating polyradiculoneuropathy.
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Free Research Field |
神経内科学
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Academic Significance and Societal Importance of the Research Achievements |
希少疾患の免疫介在性脱髄性ニューロパチーでは自己抗体がほとんど同定されておらず発症メカニズは十分に解明されていない。本研究では糖脂質と蛋白複合抗原を標的とした自己抗体は検出されず、末梢神経ミエリンもしくは傍絞輪部に局在する未同定の分子が標的抗原となっている可能性が示唆された。また、慢性炎症性脱髄性多発根ニューロパチーにおけるGQ1b抗体の存在が明らかとなり、本研究結果が今後のさらなる病態解明につながる可能性がある。
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