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2017 Fiscal Year Final Research Report

Regulation of NKT cell-mediated hepatic injury in mice

Research Project

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Project/Area Number 26460990
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Gastroenterology
Research InstitutionKitasato University (2017)
Niigata University (2014-2016)

Principal Investigator

Kawamura Toshihiko  北里大学, 医療衛生学部, 教授 (70301182)

Co-Investigator(Kenkyū-buntansha) 神田 泰洋  新潟大学, 医歯学系, 助教 (00436768)
Project Period (FY) 2014-04-01 – 2018-03-31
KeywordsNKT細胞 / 肝炎 / alpha-galactosylceramide / RASAL3 / 骨髄由来抑制細胞
Outline of Final Research Achievements

Treatment of mice with alpha-galactosylcermide, a specific agonist for NKT cells, induces liver injury. To investigate the mechanisms of a-GalCer induced liver injury, we focused on two factors, RASAL3 and MDSC(Myeloid-derive suppressor cells).
1. RASAL3 which is a hematopoietic RasGAP protein, was found to be predominantly expressed in liver NKT cells. Analysis of RASAL3-deficient mice demonstrated that RASAL3 contributes to aggravation of liver injury by regulating NKT cell function.
2. The number of myeloid-derive suppressor cells (MDSC) was increased in the liver of a-GalCer treated mice. These MDCS were found to suppress liver injury by regulating NKT cell activation through the production of inhibitory cytokines.

Free Research Field

肝臓病学

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Published: 2019-03-29  

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