Study on the role of TLR3 in radiation-induced gastrointestinal syndrome
Project/Area Number |
25870165
|
Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Multi-year Fund |
Research Field |
Immunology
Pathological medical chemistry
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Research Institution | The University of Tokyo |
Principal Investigator |
Takemura Naoki 東京大学, 医科学研究所, 特任助教 (50648699)
|
Project Period (FY) |
2013-04-01 – 2016-03-31
|
Project Status |
Completed (Fiscal Year 2015)
|
Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
|
Keywords | 自然免疫 / 急性放射線性消化管症候群 / TLR3 / 小腸陰窩 / 細胞死 / p53 |
Outline of Final Research Achievements |
Gastrointestinal syndrome (GIS) is an acute illness that occurs owing to collapse of intestinal epithelium upon exposure to high amounts of ionizing radiation in nuclear accident or cancer treatment. In this research, we identified that mice deficient in the innate immune receptor Toll-like receptor 3 (TLR3) show substantial resistance to GIS and that an inhibitor of TLR3-RNA binding also ameliorates GIS, suggesting the critical role of TLR3 in the pathogenesis of GIS. We also revealed that, TLR3 induces extensive cell death in small intestinal crypt following the crypt cell death initially induced by irradiation, aggravating destruction of intestinal epithelium. These findings will provide new therapeutic strategies targeting innate immunity for the prevention of GIS.
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Report
(4 results)
Research Products
(27 results)