| Project/Area Number |
18590467
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Immunology
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| Research Institution | Chiba University |
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Principal Investigator |
SAKAMOTO Akemi Chiba University, Graduate School of Medicine, Assistant Professor (90359597)
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| Co-Investigator(Kenkyū-buntansha) |
TOKUHISA Takeshi Chiba University, Graduate School of Medicine, Professor (20134364)
HATANO Masahiko Chiba University, Graduate School of Medicine, Professor (20208523)
ARIMA Masafumi Chiba University, Graduate School of Medicine, Lecturer (00202763)
FUJIMURA Risa Chiba University, Biomedical Research Center, Assistant Prof. (30376363)
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| Project Period (FY) |
2006 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥4,020,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥420,000)
Fiscal Year 2007: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2006: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | Immunology / allergy / target gene / gene regulation / development / 発王制御 / BCL6 / 樹状細胞 / 転写因子 / サイトカイン / BCL6欠損マウス / CD8陽性樹状細胞 / CD4陽性樹状細胞 / 抗原提示細胞 |
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| Research Abstract |
Bcl6-deficient mice display Th2-type inflammation and dendritic cells (DCs) are critical to induce Th1/2 cells. However, function of Bcl6-deficient DCs has never been discussed.
We examined a role of Bcl6 in DC generation and function in this study. 1. The number of CD11c^<high> conventional DCs (cDCs) including CD8α^+ and CD4^+ DC subsets but not that of B220^+ mPDCA-1^+ plasmacytoid DCs (pDCs) was markedly reduced in the spleen of Bcl6-deficent mice. 2. Generation of cDCs but not that of pDCs was perturbed in BM chimerical mice. 3. Precursor (CD24^+CD11b^<low>) cells of CD8α^+ cDCs derived from Bcl6-deficient BM cells stimulated with Flt3L were apoptotic more than those from wild type BM cells. 4. High level of Bcl6 mRNA was detected in splenic CD4^+ and CD8α^+ cDCs. 5. LPS-activated Bcl6-deficient DCs produced IL-6 and induced Th2 cells more than LPS-activated wild type DCs did.
Taken together Bcl6 in DC precursor cells is required for generation of CD4^+ and CD8α^+ cDCs and DCs might be one of the cause of Th2-type inflammation in Bcl6-deficient mice.
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