| Project/Area Number |
17K09616
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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 |
Respiratory organ internal medicine
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| Research Institution | Okayama University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
大藤 剛宏 岡山大学, 大学病院, 教授 (40452578)
前田 嘉信 岡山大学, 医歯薬学総合研究科, 教授 (60403474)
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2019: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2018: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 閉塞性細気管支炎 / マクロファージ / 同種造血幹細胞移植 |
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| Outline of Final Research Achievements |
Bronchiolitis obliterans syndrome (BOS) remain one of the most devastating complications in hematopoietic cell transplantation (HCT). We studied infiltrated macrophages in gender mismatched HCT recipients who received lung transplantation for BOS. We found that most of the infiltrated macrophages are derived from donor. As for phenotypes, the macrophages in early stage of BOS were positive for CD68 and iNOS and negative for CD163, CD206, and TGF-β suggesting M1 macrophages. On the other hand, neither CD68 and iNOS nor CD163, CD206, and TGF-β was negative in late stage.
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| Academic Significance and Societal Importance of the Research Achievements |
BOSは肺の慢性移植片対宿主病と考えられおり、ドナーリンパ球を主な標的とした治療が実施されるも効果は限定的であった。そのため、原疾患が完治した後にも、患者のQOLおよび予後を著しく害する合併症であり、新規治療が待たれている。今回の検討から、造血幹細胞由来のドナー型マクロファージを標的とした治療が新しい治療戦略となる可能性が考えられた。
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