| Project/Area Number |
17390139
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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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 |
NAKAYAMA Toshinori Chiba University, Graduate School of Medicine, Professor (50237468)
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| Co-Investigator(Kenkyū-buntansha) |
細川 裕之 千葉大学, 大学院医学研究院, 助手 (60431756)
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| Project Period (FY) |
2005 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥15,340,000 (Direct Cost: ¥14,500,000、Indirect Cost: ¥840,000)
Fiscal Year 2007: ¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2006: ¥4,200,000 (Direct Cost: ¥4,200,000)
Fiscal Year 2005: ¥7,500,000 (Direct Cost: ¥7,500,000)
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| Keywords | Immunology / Chromatin remodeling / Allergy / Asthma / Memory T cell / Polycomb / Trithorax / 発生・分化 |
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| Research Abstract |
T helper type 2 (Th2) cells produce IL-4, IL-5, and IL-13, and play an important role in humoral immunity and allergic reactions. During Th2 cell differentiation, naive CD4 T cells acquire "Th2 cell identity", I. e., the capability to produce selectively a large amount of Th2 cytokines. Th2 cell identity is maintained in memory Th2 cells. The expression of GATA3, a master transcription factor for Th2 cell differentiation, is uniquely regulated by several distinct mechanisms. The maintenance of transcriptional expression of the GATA3 and Th2 cytokine genes in established Th2 cells including memory Th2 cells is epigenetically regulated by a Trithorax group gene, MLL (Yamashita, et. Al. Immunity, 2006). A Polycomb group gene Bmi1 supports memory Th1/Th2 cell survival via the repression of the expression of the Noxa gene (Yamashita, et. Al. J. Exp. Med. In press). Molecular analyses of memory Th2 cells revealed that cell survival and the maintenance of Th2 cell function are epigenetically regulated by various nuclear factors, including Polycomb and Trithorax molecules.
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