| Project/Area Number |
12670621
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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) |
NAKANO Hideki Toho University, Sch. Med., Dept. Immunol., Lecturer, 医学部, 講師 (30266928)
IWASAKI Yasuo Toho University, Sch. Med., 4th Dept. Med., Assoc. Prof., 医学部, 助教授 (30130347)
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| Project Period (FY) |
2000 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2002: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 2001: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2000: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | plt mouse / SLC chemokine / ELC chemokine / experimental allergic encephalitis / T cell / regulation of T cell response / multiple sclerosis / 実験的アレルギー性脳脊髄炎 |
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| Research Abstract |
Experimental allergic encephalitis (EAE) is a mouse model of human multiplesclerosis. Paucity of lymph node T cells (plt) mouse lacks expression of SLC (CCL21) and ELC (CCL19) chemokines. Immunization with MOG peptide induces experimental allergic encephalitis in control mice, but not in plt mice. When T cells were transferred from +/plt-C56BL/6mice immunized with MOG peptide into pltmice, EAE was deloped, suggesting that failure to develop EAE in pltmice was not due to migration failure induced by lacking chemokine expression, but due to effector T cell development
pltmice lack expression of SLC and ELC chemokines, but T cell response to subcutaneous immunization with a protein antigen was rather higher than in control mice and prolonged much longer than in control mice. These findings suggest that T cell immune regulation is insufficient in pltmice. Apoptosis in draining lymph mode in pltmice was much less evident in pltmice than in control mice, which resulted in keeping increased number of responding T cells. To elucidate the mechanisms for the failure to develop EAE in pltmice, we will analyze effector CD4+ T cells after immunization with protein antigen
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