| Project/Area Number |
12660110
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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 |
食品科学・栄養科学
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| Research Institution | THE UNIVERSITY OF TOKYO |
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Principal Investigator |
HACHIMURA Satoshi GRADUATE SCHOOL OF AGRICUlTURAL AND LIFE SCIENCES, THE UNIVERSITY OF TOKYO, ASSOCIATE PROFESSOR, 大学院・農学生命科学研究科, 助教授 (40238019)
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| Co-Investigator(Kenkyū-buntansha) |
KAMINOGAWA Shuichi GRADUATE SCHOOL OF AGRICUlTURAL AND LIFE SCIENCES, THE UNIVERSITY OF TOKYO, PROFESSOR, 大学院・農学生命科学研究科, 教授 (50011945)
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 2001: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 2000: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | intestinal immune response / Peyer's patch / oral tolerance / T cell / signal transduction / dendritic cell / interleukin 5 / interleukin 6 |
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| Research Abstract |
1. Interlaken (IL) -5 and IL-6 secretion of Peyer's patch cells. (1) It was demonstrated that PP dendritic cells (DCs), particularly CD11b^+ DCs produced higher levels of IL-6 compared to SP DCs. (2) We found that naive CD4 T cells had a high capacity to secrete IL-6. (3) We found that IL-2R^+ CD3^-B220^- non T, non-B cells isolated from PP cells secreted IL-5 in response to IL-2. These IL-2R^+ cells did not belong to previously known IL-5 producing cells, such as T cells, mast cells, NK cells or eosinophils. Deoletion of IL-2R^+CD3^-B220^- cells from PP cells resulted in reduced IL-5 production.
2. Signal transduction pathways in orally tolerant CD4 T cells induced in ovalbumin-specific T cell receptor (TCR) transgenic mice fed with ovalbumin was examined. In these T cells (1) impaired phosphorylation of TCR-ζ, ZAP-70, LAT (2) impaired calcium responses and decreased NFAT nuclear translocation, (3) normal activation of ERK and SAPK (MAPK pathway), and (4) impaired degradation of p27^<kip1> induced by IL-2 stimulation was demonstrated. Thus, hyporesponsiveness in the orally tolerant CD4 T cell appears to be associated with two defects : impaired TCR-induced activation of the calcium pathway, and impaired p27 ^<kip1> degradation induced by stimulation thorough IL-2R.
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