The blistering mechanisms in bullous pemphigoid
Project/Area Number |
26860861
|
Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Dermatology
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Research Institution | Hokkaido University |
Principal Investigator |
Iwata Hiroaki 北海道大学, 大学病院, 特任助教 (20397334)
|
Project Period (FY) |
2014-04-01 – 2016-03-31
|
Project Status |
Completed (Fiscal Year 2015)
|
Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2015: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
|
Keywords | 自己免疫 / 自己抗原 / 水疱性類天疱瘡 / 17型コラーゲン / 自己免疫疾患 / 自己抗体 / エンドサイトーシス / 自己免疫性疾患 / Trim21 / ユビキチン |
Outline of Final Research Achievements |
Bullous pemphigoid (BP) is an autoimmune subepidermal blistering disease associated with autoantibodies to type XVII collagen (COL17). When keratinocytes are treated with BP-IgG, COL17 internalizes into cells by way of the macropinocytosis pathway. The inhibition of small GTPase family members Rac1 and Cdc42 was found to strongly repress COL17 internalization; additionally the Rho inhibitor also partially blocked the internalization.This depletion of COL17 from lateral-apical plasma membrane generates a significant shortage of COL17-supplementation to hemidesmosome, resulting in the formation of incomplete hemidesmsome lacking COL17.
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Report
(3 results)
Research Products
(2 results)