| Project/Area Number |
13660318
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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 |
Applied veterinary science
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| Research Institution | Yamaguchi University |
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Principal Investigator |
HAYASHI Toshiharu Facultyof Agriculture, Yamaguchi University, Professor, 農学部, 教授 (90111484)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥2,900,000 (Direct Cost: ¥2,900,000)
Fiscal Year 2002: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2001: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | Th1 / Th2 / Reovirus type-2 / Insulitis / Autoimmune diabetes / Gene therapy / ループス / インターフェロンーガンマ / IL-4 / IL-18 / IL-12 / DNAワクチン / レオウイルスー2型 / 自己免疫 / 唾液腺炎 / ラミニン / 全身性エリテマトーデス / アレルギー性気管支炎 |
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| Research Abstract |
Summary consisted of 10 items listed bellow concerning gene therapy for autoimmune diabetes by DNA vaccine. (1)Th1-dominant systemic immune responses, being responsible for the development of autoimmune insulitis, might be induced by IL-12-induced and IL-18-activated mechanisms. (2)Laminin expression is associated with the cellular infiltration of the submandibular salivary gland of NZBxNZWf1 mice. (3) The reduced bronchial lesions in C57BL/6 mice were due, at least in part, to suppression of the Th2 immune response that underlies the decreased infiltration of lymphocytes and eosinophils into the bronchial mucosa. (4) Increase in serum IFN-r may be associated with the active disease in NZBxNZWF1 mice. (5) The insulitis seen in Reo-2 infection in suckling mice is induced by an immune reaction. (6) The systemic administration of IFN-r-expressing plasmid may have a modulating ability of Th1/Th2 balance to down-regulate Th2 response by mutual inhibitoru mechanisms between Th1 and Th2 cells, leading to the reduction of th LAR. (7) IFN-r but not IL-4 contribute to the development of lupus in the NZBxNZWF1 mice. (8) The IFN-r-encoding plasmid promoted autoimmune insulitis in Reo-2-induced diabetes. (9) CpG ODN may contribute to accelerate Reo-2-induced autoimmune reaction against pancreatic islet cells via additional effects of Th1 cytokine especially IFN-r. (10) ICAM-1/LFA-1 may be required for the differentiation of Th0 cells to Th1 cells, which mediate insulitis with IGT in Reo-2-infected suckling mice.
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