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KAKEN_25860967seika.pdf
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菌状息肉症モデルマウスの作製と表皮浸潤・転移機構の解析
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キンジョウ ソクニクショウ モデル マウス ノ サクセイ ト ヒョウヒ シンジュン・テンイ キコウ ノ カイセキ
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Kinjo sokunikusho moderu mausu no sakusei to hyohi shinjun teni kiko no kaiseki
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The study of mechanism of epidermotropism and metastasis of mycosis fungoides by establishing mouse mycosis fungoides model
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福田, 桂太郎
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フクダ, ケイタロウ
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Fukuda, Keitaro
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慶應義塾大学・医学部・特任助教
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Research team head
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科研費研究者番号 : 60464848
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2015
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科学研究費補助金研究成果報告書
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2014
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菌状息肉症(MF)は表皮向性を示し, interface dermatitis(ID)やPautrier微小膿瘍(PM)を認める。本研究はMFマウスの作製, MFの表皮浸潤機構の解明を目的に実施した。我々はデスモグレイン3を認識するTCR(H1), MFのInk4a/Arf(がん抑制遺伝子)変異, c-Myc(がん遺伝子)をCD4+T細胞に導入, Rag2欠損マウスに移植し, ID, PMをきたすMFマウスの作製に成功した。Ink4a/Arf変異・H1導入CD4+細胞はPMを形成せず, Ink4a/Arf変異・c-Myc導入CD4+T細胞はPMを形成した。PMの形成にはc-Mycが必要であることが示唆された。
Mycosis fungoides (MF) is a cutaneous T cell lymphoma of CD4+ T cells that show epidermotropism. It is characterized by interface dermatitis (ID) and Pautrier's microabscess (PM), a clustering of MF cells in the epidermis. This project was conducted to establish MF model mouse that recapitulate histopathology of MF and to clarify the mechanism of the development of PM. Since mutation in INK4A/ARF (tumor suppressor gene) and overexpression of C-MYC (oncogene) are associated in human MF, we isolated CD4+T cells from Ink4/Arf-/- mice and retrovirally transduced c-Myc and desmoglein 3 specific TCR (H1) that induces ID. T cells were then adoptively transferred into Rag2-/- mice, which lead to the development of ID and PM that recapitulated MF. In addition, transfer of Ink4/Arf-/- CD4+T cells transduced with c-Myc developed PM whereas transfer of Ink4/Arf-/- CD4+T cells transduced with H1 did not develop PM. Our results suggest that oncogene c-Myc is essential for the development of PM.
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研究種目 : 若手研究(B)
研究期間 : 2013~2014
課題番号 : 25860967
研究分野 : 皮膚科学
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May 7, 2020 | | Creator,Abstract 内容,Note 注記 を変更 |
May 7, 2020 | | Creator 著者ID を変更 |
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