role of HMGB-1-RAGE pathway on acute GVHD
| Project/Area Number |
24591424
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Hematology
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| Research Institution | Okayama University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
TANIMOTO Mitsune 岡山大学, 医歯薬学総合研究科, 教授 (10240805)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | GVHD |
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| Outline of Final Research Achievements |
Tissue damage caused by the conditioning regimen leads to the release of exogenous and endogenous “danger signals”. Exogenous danger signals called pathogen-associated molecular patterns (PAMPs) and endogenous noninfectious molecules known as damage-associated molecular patterns (DAMPs) are responsible for initiating or amplifying acute GVHD by enhancing DC maturation and alloreactive T-cell responses. High mobility group box 1 protein (HMGB1) is expressed ubiquitously and located mostly in cell nuclei. HMGB1 is released on tissue damage as an endogenous DAMP and is actively produced by immune cells. We investigated the effects HMGB1 on a well-defined chronic GVHD mice model. There was a significant difference in GVHD damage between allogeneic recipient control mice and those lacking one of receptor HMGB1, RAGE. Anti HMGB1 Ab reduced GVHD damage in recipient mice.
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Report
(4 results)
Research Products
(2 results)
