Pathogenesis of bullous pemphigoid: a study using class-switched monoclonal antibodies.
| Project/Area Number |
16K15539
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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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 |
Nishie Wataru 北海道大学, 医学研究科, 准教授 (20443955)
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| Co-Investigator(Kenkyū-buntansha) |
夏賀 健 北海道大学, 大学病院, 講師 (70645457)
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 皮膚病態学 / 皮膚病態斈 |
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| Outline of Final Research Achievements |
Bullous pemphigoid (BP) is an autoimmune blistering skin disease, in which autoantibodies target collagen XVII (COL17) in the skin. Here we produced recombinant monoclonal antibodies (mAb) directing COL17 with different isotypes including IgG1, IgG2a, IgA and IgE. These mAbs have identical variable regions. Passive transfer of these mAbs into mice induced activation of complements when IgG2a but not IgG1 mAbs were injected. However, there was no clinical differences were observed in complement-activating and complement-non-activating recipient mice. These results suggest that activation of complements is not enough to induce blistering skin disease in mice.
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Report
(3 results)
Research Products
(5 results)
