| Project/Area Number |
26460078
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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 |
Biological pharmacy
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| Research Institution | Tokyo University of Science |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
Ichiro Horie 東京理科大学, 薬学部, 助教 (10609514)
Masanori Shinohara 熊本大学, 生命科学研究部, 教授 (90117127)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | シェーグレン症候群 / 自己抗体 / アクアポリン / 視神経脊髄炎 |
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| Outline of Final Research Achievements |
Sjogren's syndrome (SjS), is an autoimmune disease targeting exocrine glands, which results in severe dry mouth and eyes. Specific autoantibodies to cause the pathogenesis in SjS have not been identified. Aquaporin-5 (AQP5) water channel, is selectively expressed in exocrine glands, and enhances fluid secretion. We, thereofore, hypothesized that SjS patients have autoantibodies against AQP5. To prove this hypothesis, in this study, we examined the immunoreactivity of sera and IgG fractions from SjS patients, against AQP5-expressing cells. Interestingly, 60% of SjS sera and IgG showed specific immunoreactivity in AQP5 expressing cells. In addition, SjS-IgG significantly decreased water permeability trough AQP5, and caused internalization of AQP5. These results suggest that autoantibodies against AQP5 may be involved in the pathogenesis of SjS, by inhibiting AQP5 function and cell surface expression.
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