| Project/Area Number |
18K15454
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 52020:Neurology-related
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| Research Institution | Kyushu University |
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Principal Investigator |
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| Project Period (FY) |
2018-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2019: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2018: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | Neurofascin 155 / ランビエ絞輪 / IgG4 / 慢性炎症性脱髄性多発神経炎 / Contactin-1 / 自己抗体 / ニューロパチー / neurofascin 155 / CIDP / contactin-1 / caspr-1 / 慢性炎症性脱髄性多発ニューロパチー / contactin 1 / Caspr-1 / 神経免疫 |
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| Outline of Final Research Achievements |
Autoantibodies against paranodal proteins, such as neurofascin 155 (NF155) and contactin-1 (CNTN1), have been reported in subsets of chronic inflammatory demyelinating polyneuropathy (CIDP). Through the research, we identified one anti-CNTN1 antibody-positive CIDP patient, who concurrently had membranous nephropathy. We also demonstrated strong associations with human leukocyte antigen (HLA), particularly HLA class II alleles, in IgG4 anti-NF155 antibody-positive CIDP. Then we showed that intrathecal upregulation of type 2 helper T cell cytokines is characteristic of IgG4 anti-NF155 antibody-positive CIDP, while type 1 helper T cell cytokines are increased in CIDP regardless of the presence or absence of anti-NF155 antibodies.
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| Academic Significance and Societal Importance of the Research Achievements |
抗CNTN1抗体陽性CIDPの存在は、蛋白間相互作用によりCIDPを発症するという仮説を支持するものである。今回同定した抗CNTN1抗体陽性CIDP症例は同時に膜性腎症を合併しており、CIDPおよび膜性腎症の発症機序の共通点を見出す上で非常に重要である。また、本研究を通してこれまでにない規模でIgG4抗NF155抗体陽性CIDPの免疫遺伝学的な背景を明らかにすることができた。Th2およびその関連サイトカインは今後、治療標的と成り得る。
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