| Project/Area Number |
25461450
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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 | Osaka University |
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Principal Investigator |
Fukushima Kentaro 大阪大学, 医学(系)研究科(研究院), 招聘教員 (70546879)
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| Co-Investigator(Kenkyū-buntansha) |
YOKOTA Takafumi 大阪大学, 大学院医学系研究科, 助教 (60403200)
ORITANI Kenji 大阪大学, 大学院医学系研究科, 准教授 (70324762)
KANAKURA Yuzuru 大阪大学, 大学院医学系研究科, 教授 (20177489)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 免疫寛容 / リンパ球造血 / 造血幹細胞 / リンパ球分化 / リンパ球の分化・増殖 |
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| Outline of Final Research Achievements |
Mammals have evolved to protect their offspring during early fetal development. Although fetuses represent mismatched allografts because of paternal genes, they develop with remarkable speed by obtaining optimal nutrition through the placenta. Thus, elaborate mechanisms induce tolerance of maternal immune system. We found that estrogen-induced Frizzled-related proteins (sFRPs), particularly sFRP5, suppress B-lymphopoiesis in vivo. Mice overexpressing sFRP5 had fewer B-lymphocytes in the peripheral blood and spleen. High levels of sFRP5 inhibited early B-cell differentiation in the bone marrow (BM), resulting in the accumulation of cells with a common lymphoid progenitor (CLP) phenotype. Conversely, sFRP5 deficiency reduced the number of hematopoietic stem cells and primitive lymphoid progenitors in the BM, particularly when estrogen was administered. Furthermore, a significant reduction in CLPs and B-lineage-committed progenitors was observed in the BM of sfrp5-null pregnant females.
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