The elucidation of novel T cell function in innate immunity-dominated liver tissue damage.
| Project/Area Number |
25670590
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Digestive surgery
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| Research Institution | The Tazuke Kofukai |
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Principal Investigator |
TERAJIMA Hiroaki 公益財団法人田附興風会, 医学研究所 第1研究部, 研究主幹 (40314215)
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| Co-Investigator(Kenkyū-buntansha) |
UCHIDA Yoichiro 公益財団法人田附興風会, 医学研究所第1研究部, 主任研究員 (30597745)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 肝虚血再灌流障害 / galectin-9 / Tim-3 / 虚血再還流障害 / 肝臓 / T細胞 / TIM-3 / TLR-4 / マクロファージ / 虚血再灌流障害 / TIM / Galectin-9 |
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| Outline of Final Research Achievements |
Liver ischemia reperfusion injury (IRI) is still an important problem in liver transplantation, and is affected by T-cell / Macrophage interaction. We have focused on Tim-3 / Galectin-9 pathway as regulatory system in liver IRI. The expression of Gal-9 was enhanced endogenously in liver especially by hepatocytes and Kupffer cells during warm IRI for a mouse liver. Exogenously administered reGal-9 significantly ameliorated hepatocellular damage due to IR. In the circumstance of Gal-9 absence, the liver damage exacerbated the severity as compared with wild type. The severe liver damage in Gal-9 KO mice was improved by the administration of reGal-9. Our study suggests a significant role of Gal-9 in the maintenance of hepatic homeostasis, and exogenous Gal-9 treatment will be a new therapeutic strategy against liver IRI.
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Report
(4 results)
Research Products
(2 results)
