2017 Fiscal Year Final Research Report
Regulation of NKT cell-mediated hepatic injury in mice
Project/Area Number |
26460990
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Gastroenterology
|
Research Institution | Kitasato University (2017) Niigata University (2014-2016) |
Principal Investigator |
|
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
|
Keywords | NKT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.
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Free Research Field |
肝臓病学
|