| Project/Area Number |
17K10230
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Dermatology
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| Research Institution | Gunma University |
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Principal Investigator |
Kishi Chikako 群馬大学, 医学部附属病院, 講師 (60402707)
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| Co-Investigator(Kenkyū-buntansha) |
天野 博雄 岩手医科大学, 医学部, 教授 (70302487)
茂木 精一郎 群馬大学, 大学院医学系研究科, 准教授 (20420185)
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2019: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2018: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2017: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | アトピー性皮膚炎 / NK細胞 |
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| Outline of Final Research Achievements |
We studied the mechanism of parasite infection of NC/Nga mice, which are models of atopic dermatitis, in order to elucidate the mechanism of suppression of the onset of dermatitis and improvement of symptoms, and to develop an effective treatment for atopic dermatitis. Infection of NC/Nga mice with malaria resulted in an increase in NK cells locally in the skin and improved eczema lesions. The removal of NK cells by anti-acyaro-GM1 antibody did not improve the malaria-induced skin lesion. Next, NK cells were isolated from the spleen of malaria-infected NC/Nga mice and administered transvenously to malaria-free NC/Nga mice with eczema to investigate dermatitis.
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| Academic Significance and Societal Importance of the Research Achievements |
今回の成果によって、十分に明らかになっていなかったアトピー性皮膚炎発症機序の一部にＮＫ細胞が関与することが示唆された。皮膚炎の発症の抑制、症状の軽快が生じるメカニズムを実験的に解明することができ、今後、アトピー性皮膚炎をはじめとするアレルギー疾患の有効な治療法に繋がることが期待される。また、今回の研究成果は、アトピー性皮膚炎の衛星仮説の機序の解明にもつながる成果である。
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