The elucidation of novel T cell function in innate immunity-dominated liver tissue damage.

2015 Fiscal Year Final Research Report

• Project/Area Number: 25670590
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: Digestive surgery
• Research Institution: The Tazuke Kofukai
• 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)
• 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)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: 肝虚血再灌流障害 / galectin-9 / Tim-3

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.

Free Research Field

医歯薬学