| Project/Area Number |
21590859
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Gastroenterology
|
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| Research Institution | Juntendo University |
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Principal Investigator |
IKEJIMA Kenichi 順天堂大学, 医学(系)・研究科(研究院), 准教授 (20317382)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
YAMASHINA Shunhei 順天堂大学, 医学部, 准教授 (30338412)
KON Kazyyoshi 順天堂大学, 医学部, 准教授 (30398672)
|
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| Co-Investigator(Renkei-kenkyūsha) |
TAKEDA Kazuyoshi 順天堂大学, 医学部, 准教授 (80272821)
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| Project Period (FY) |
2009 – 2011
|
| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2011: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2010: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2009: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | 非アルコール性脂肪肝炎(NASH) / 自然免疫 / メタボリックシンドローム / NKT細胞 / 肝線維化 / 肝再生 / NK細胞 / CD1d / アディポカイン / チアゾリジン系誘導体 |
|---|
| Research Abstract |
Recent lines of evidence support the hypothesis that innate immune system plays a pivotal role in pathogenesis of nonalcoholic steatohepatitis. In this study, we found that KK-Ay mice, which present metabolic syndrome-like phenotypes, show progressive depletion of hepatic natural killer T(NKT) cells in combination with functional abnormalities. On the other hand, CD1d-knockout(KO) mice, in which NKT cells are systemically defective, develop minimal hepatic fibrosis caused by thioacetamide. Further, deprivation of NK and NKT cells using an NK1.1 antibody resulted in impaired regenerative response following partial hepatectomy. Collectively, these findings indicate that hepatic NKT cells are required for tissue-repair and fibrogenic responses in the liver.
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