| Project/Area Number |
16616001
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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 |
アレルギー
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| Research Institution | Chiba University |
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Principal Investigator |
SAKAMOTO Akemi Chiba University, Graduate School of Medicine, Assistant Prof., 大学院・医学研究院, 助手 (90359597)
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| Co-Investigator(Kenkyū-buntansha) |
TOKUHISA Takeshi Chiba University, Graduate School of Medicine, Professor, 大学院・医学研究院, 教授 (20134364)
HATANO Masahiko Chiba University, Gene Research Center, Associate Prof., バイオメディカル研究センター, 助教授 (20208523)
ARIMA Masafumi Chiba University, Graduate School of Medicine, Lecturer, 大学院・医学研究院, 講師 (00202763)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥3,700,000 (Direct Cost: ¥3,700,000)
Fiscal Year 2005: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2004: ¥2,300,000 (Direct Cost: ¥2,300,000)
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| Keywords | allergy / Bcl6 / dendritic cells / regulation of gene expression / development differentiation / BAZF / gene-deficient mice / Th2炎症 / 遣伝子欠損マウス / CD4T細胞 |
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| Research Abstract |
The Bcl6 gene is ubiquitously expressed in heamatopoietic cells and Bcl6-deficient mice displayed eosinophilic inflammation caused by overproduction of Th2 cytokines. In the spleen of Bcl6-deficient mice, T1/ST2^+ Th2 CD4 T cells detected more than wild type mice but responsible cells of this Th2 skewing were suggested as non T cell by transfer experiment.
In this study, we analyzed subpopulation of dendritic cells (DC) in spleen of Bcl6-deficient mice. We found the number of CD11c^+ DC was reduced and proportion of CD8^+ DC, CD4^+ DC were dramatically reduced. From analysis of bone marrow chimeric mice and bone marrow derived DC, we concluded that abnormality of DC differentiation was caused by DC progenitor at DC precursor level. Then Bcl6 is essential for CD8^+ and CD4^+ DC development.
Next we analyzed the ability of Th2 skewing by Bcl6-deficient DC. Bone marrow derived DC from Bcl6-deficient induced T1/ST2^+ CD4 T cells more than wild type DC in the culture condition. These results indicated that Bcl6-deficient DC was one of the responsible cells of Th2 skewing of Bcl6-deficient mice.
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