| Project/Area Number |
21390086
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General medical chemistry
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| Research Institution | Fukushima Medical University |
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Principal Investigator |
FUJITA Teizo 福島県立医科大学, 医学部, 名誉教授 (20134223)
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| Co-Investigator(Kenkyū-buntansha) |
IWAKI Daisuke 福島県立医科大学, 医学部, 助教 (10315492)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥16,640,000 (Direct Cost: ¥12,800,000、Indirect Cost: ¥3,840,000)
Fiscal Year 2011: ¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2010: ¥6,500,000 (Direct Cost: ¥5,000,000、Indirect Cost: ¥1,500,000)
Fiscal Year 2009: ¥6,370,000 (Direct Cost: ¥4,900,000、Indirect Cost: ¥1,470,000)
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| Keywords | 免疫学 / 自然免疫 / 補体 / レクチン経路 / 第2経路 / MASP / 感染症 / 生体分子 / 糖鎖 / 凝固系 |
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| Research Abstract |
In the lectin pathway, mannose-binding lectin(MBL) and ficolins act as pattern recognition molecules for pathogens, resulting in the activation of MBL-associated serine proteases(MASPs ; MASP-1, MASP-2 and MASP-3). Among these proteases, MASP-2 is thought to be a key enzyme that cleaves C4 and C2 to assemble a C3 convertase(C4b2a). However, a physiological function of MASP-1 and MASP-3 remains unclear. To investigate the roles of MASP-1 and MASP-3, we generated a MASP-1-and MASP-3-deficient mouse model, and found that the deficient mice lacked alternative pathway activation, because Df remained as a proenzyme in the serum. MASP-1 and MASP-3 were able to convert the proenzyme of Df to an active form in vitro. In addition, MASP-3 was able to activate Bf of the alternative pathway. Thus, MASP-1 and MASP-3 seems to be involved in activation of both the lectin and alternative pathways, thereby, playing a central role in innate immunity.
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