2017 Fiscal Year Final Research Report
Analysis of cutaneous lesion in collagen disease induced by intranuclear autoantibody.
Project/Area Number |
15K09790
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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 |
Research Field |
Dermatology
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Research Institution | Toho University |
Principal Investigator |
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Co-Investigator(Kenkyū-buntansha) |
井川 健 獨協医科大学, 医学部, 教授 (00372441)
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Co-Investigator(Renkei-kenkyūsha) |
TSUBATA Takeshi 東京医科歯科大学, 難治疾患研究所, 教授 (80197756)
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Project Period (FY) |
2015-04-01 – 2018-03-31
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Keywords | CD40リガンド / トランスジェニックマウス / アトピー性皮膚炎 / 脱毛症 |
Outline of Final Research Achievements |
Vk38c type VL chain, derived from CD40 ligand transgenic (Tg) mouse, was observed in anti-Sm/RNPab, and dermatitis and alopecia were observed in Vk38c Tg mouse. Under conventional condition, dermatitis in Vk38g Tg mice was enhanced, and intraepidermal inflammation similar to eczematous reaction was observed in histology. In these mice serum IgE levels were elevated. In alopecia lesion induced by skin inflammation, lymphocytic inflammation was augmented in histology. In contrast, histological finding of alopecia lesion of Vkc Tg mouse kept long-term in conventional condition was similar to human alopecia aleata, lacking inflammation and epidermal proliferation. It is suggested that autoantibody in Vk38c Tg mouse influenced the histological difference of dermatitis and alopecia, in conventional conditions.
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Free Research Field |
皮膚免疫・アレルギー
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