2015 Fiscal Year Final Research Report
The blistering mechanisms in bullous pemphigoid
| Project/Area Number |
26860861
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Dermatology
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| Research Institution | Hokkaido University |
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Principal Investigator |
Iwata Hiroaki 北海道大学, 大学病院, 特任助教 (20397334)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Keywords | 自己免疫 / 自己抗原 / 水疱性類天疱瘡 / 17型コラーゲン |
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| 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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| Free Research Field |
自己免疫性水疱症
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