| Project/Area Number |
15K19893
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Digestive surgery
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| Research Institution | Hiroshima University |
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Principal Investigator |
Ohira Masahiro 広島大学, 病院(医), 病院助教 (30397947)
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | NK細胞 / TRAIL / ケモカイン / 肝切除 / 肝癌 |
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| Outline of Final Research Achievements |
Liver resident natural killer (NK) cells express tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), a critical molecule for NK cell-mediated tumor cell killing.
TRAIL+ NK cells strongly and exclusively expressed CXCR3. CXCL9, a ligand of CXCR3, was significantly decreased in the liver after hepatectomy. The kinetics of hepatic CXCL9 expression resembled those of hepatic TRAIL+ NK cell proportions after hepatectomy. Among liver-resident mononuclear cells, macrophages predominantly secreted CXCL9 in response to interferon (IFN)-gamma stimulation. Although the administration of poly I:C, an inducer of IFN-gamma, increased hepatic CXCL9 levels in both CXCR3-/- and WT mice, even after hepatectomy, only WT mice recovered TRAIL expression on NK cells. Major hepatectomy remarkably reduced the proportion of TRAIL-expressing NK cells in the liver through downregulation of the CXCL9-CXCR3 axis in mice.
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