| Project/Area Number |
26461498
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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 |
Infectious disease medicine
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| Research Institution | Yamagata University |
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Principal Investigator |
ABE Shuichi 山形大学, 医学部, 非常勤講師 (40400543)
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| Co-Investigator(Renkei-kenkyūsha) |
SHIBATA Yoko 山形大学, 医学部, 講師 (60333978)
KIMURA Tomomi 山形大学, 医学部, 医員 (50536935)
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| Research Collaborator |
NEMOTO Takako
SATO Masamichi
SATO Kento
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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 |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | MafB / マクロファージ / 貧食能 / Fcgr3 / 貪食 / 貪食能 / BCG |
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| Outline of Final Research Achievements |
Alveolar macrophage plays important roles in host defense against Mycobacterium tuberculosis (TB) infection in the lungs, including Fc receptor-mediated phagocytosis of TB. MafB is a transcription factor that regulates a variety of functions of macrophages. In order to assess the role of MafB in the mechanisms of phagocytosis in macrophages, we established the MafB gene-silenced macrophage cell line by gene transduction of MafB-shRNA to the macrophage cell line RAW264.7 (RAW264.7-MafB-shRNA). Fc receptor-mediated phagocytosis was suppressed by MafB gene silencing in RAW264.7 cells. Fcgr3 expression was significantly decreased in RAW264.7-MafB-shRNA compared to control cells. Forced expression of the Fcgr3 gene recovered Fc receptor-mediated phagocytosis in RAW264.7-MafB-shRNA. Our data suggested that MafB transcription factor should promote cell surface Fcgr3 expression and regulate Fc receptor-mediated phagocytosis in macrophages.
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