| Project/Area Number |
25860774
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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 |
Hematology
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| Research Institution | Hokkaido University |
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Principal Investigator |
NAKAGAWA Hisako 北海道大学, 遺伝子病制御研究所, 特任助教 (60615342)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 補体 / APS / B2GPI / 血管 |
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| Outline of Final Research Achievements |
Beta-2-glycoprotein I (B2GPI) is one of the major autoantigens in patients with anti-phospholipid syndrome (APS), an autoimmune disorder characterized by thrombosis and pregnancy morbidity. To investigate the function of anti B2GPI antibody in complement system, we asked whether anti B2GPI antibody affects the C3/B2GPI binding. Bound B2GPI and anti B2GPI to C3 was determined by ELISA. As a results, anti B2GPI antibody did not affect the C3/B2GPI binding. B2GPI and anti B2GPI antibody were added to normal human serum, complement was activated via the alternative pathway, and C5b-9 levels were determined by ELISA. B2GPI inhibited complement activation, and C5b-9 generation was reduced by ~45%. On the other hands, a significant increase in C5b-9 deposition was observed by addition of anti B2GPI antibody. We concluded that the anti B2GPI antibody regulate the effects of B2GPI in the complement system.
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