| Project/Area Number |
15590911
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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 |
Neurology
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| Research Institution | Toho University |
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Principal Investigator |
KAKIUCHI Terutaka Toho University, Sch.Med., Dept.Immunol., Professor, 医学部, 教授 (40126024)
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| Co-Investigator(Kenkyū-buntansha) |
IWASAKI Yasuo Toho University, Sch.Med., Dept.Int.Med.(Omori), Professor, 医学部, 教授 (30130347)
中野 英樹 東邦大学, 医学部, 講師 (30266928)
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| Project Period (FY) |
2003 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2004: ¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 2003: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Keywords | plt mouse / CCL21 chemokine / CCL19 chemokine / Experimental Allergic Encephalomyelitis / T cell / Regulation of T cell response / Multiple Sclerosis / SLC(CCl21)ケモカイン / ELC(CCL19)ケモカイン |
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| Research Abstract |
Experimental allergic encephalomyelitis(EAE) is an animal model for multiple sclerosis. C57BL/6 mouse immunized subcutaneously with myelin oligodendrocyte glycoprotein(MOG) 35-55 peptide(MOG35-55 peptide) in CFA developed EAE. However, C57BL/6-plt/plt mouse did not develop EAE, when similarly treated. plt mouse has a defect in the expression of CCL19/CCL21. Thus, it is possible that these chemokines are involved in the development of EAE. There were two possibilities ; one was the migration failure of pathogenic T cells into CNS, the other was that pathogenic T cells were not generated in the plt mouse. To differentiate these possibilities, T cells from C57BL/6 wild type mice immunized with MOG35-55 peptide in CFA were intravenously transferred into plt mice, which resulted in the development of EAE in plt mice. When draining lymph node cells from these mice intravenously immunized with MOG peptide in CFA, were stimulated in vitro with the peptide, T cells from plt mice produced much more IL-4 than those from wild type mice, whereas IFN-γ was inversely produced. These results, although the experiments were still preliminary, suggested that CCL19/CCL21 are involved in the generation of pathogenic Th1 cells for EAE induction. The mechanisms for the involvement of these chemokines are now under the investigation.
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