Elucidating the initial pathomechanism of bullous pemphigoid
| Project/Area Number |
23591625
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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 | Osaka City University |
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Principal Investigator |
TSURUTA DAISUKE 大阪市立大学, 医学(系)研究科(研究院), 教授 (90382043)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2013: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2011: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
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| Keywords | 水疱性類天疱瘡 / 類天疱瘡 / エンドサイトーシス |
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| Research Abstract |
The pathomechanism of the formation of bullae in bullous pemphigoid has been considered to be caused by 1) autoantibody (BP-IgG)-autoantigen (BP180) adhesion, 2) activation of complement, 3) migration of neutrophils and 4) proteolysis by neutrophil elastase. In this study, we performed live cell imaging of BP180-GFP after BP-IgG treatment on keratinocytes. The results suggested that BP180 was incorporated by macropinocytic endocytosis pathway, and that the keratinocyte cell adhesion was weakened by this pathway. We consider that this newly found initial pathomechanism of bullous pemphigoid may be the future drug target. We will be able to inhibit macropinocytosis to cure bullous pemphigoid after the drug discovery affecting it.
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Report
(4 results)
Research Products
(19 results)
