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Mechanisms and treatments of autoimmune diseases by Th1/Th2 unbalance

Mechanisms and treatments of autoimmune diseases by Th1/Th2 unbalance
Th1/Th2失衡导致自身免疫性疾病的机制及治疗
批准号:
15380210
负责人:
HAYASHI Toshiharu
金额:
$8.32万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (B)
财政年份:
2003
资助国家:
日本
项目状态:
已结题
起止时间:
2003 至 2005

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中文摘要
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英文摘要
Summary consisted of 6 items listed bellow concerning mechanisms and treatments of autoimmune diseases by Th1/Th2 unbalance[I].Lupus as Th1 disease : [1].in vivo CpG-ODN-treatment accelerated lupus nephritis during the preactive phase in lupus-prone female NZBxNZWF_1(model) mice, and IL-6 detection in the blood may be an indicator of the onset of the disease. Moreover, IFN-gamma may play a role in IL-6 production. [2].IL-1 and TNF-alfa, which are related to Th1 cytokines, may at least in part be responsible for the increased ICAM-1 expression on endothelium, in cutaneous microvessels, resulting in the vascular injury characterized by neutrophilic lekocytoclasis in B/WF1 mice. [3].CD4^+CD25^+ T cells may, at least in part, downregulate the development of glomerulonephritis during the preactive phase. [II].Type I diabete as Th1 disease. : [1] The systemic administration of IL-4 expressing plasmid DNA inhibited the development of insulitis with impaired glucose tolerance(IGT) in a dose dependent manner. [2]Adhesion molecules(ICAM-1/LFA-1) may be required for the differentiation of Th0 cells to Th1 cwlls, which mediate insulitis with IGT in Reo-2-infected suckling mice.[3].CD4^+CD25^+ T cells may, at least in part,maintain tolerance to Reo-2-triggered and CpG-ODN-induced prolonged mild Th1-depebdent auoimmune insulitis, leading to the overt diabetes.Taken together, the studies suggest that Th2-cytokine expressing plasmid may applicable for a new therapy to lupus as Th1 disease. Moreover our system may give a novel model to elucidate the mechanisms of the development of overt diabetes from borderline diabetes in virus-triggered autoimmune type I diabetes in human.
期刊论文(6)
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会议论文
ICAM-1 expression on endothelium and systemic cytokine production in cutaneous neutrophilic leucocytoclastic vasculitis in NZBxNZWF_1 mice.
NZBxNZWF_1 小鼠皮肤中性粒细胞破碎性血管炎内皮细胞 ICAM-1 表达和全身细胞因子产生。
DOI: --
发表时间: 2005
期刊: Histol.Histpatol. 20
影响因子: --
作者: [Hayashi, T., Hasegawa, K., Ichinohe, N.]
通讯作者: N.
Effect of antibodies to ICAM-1 and LFA-1 on cytokine mRNA expression in reo-2-triggered autoimmune insulitis in suckling DBA/1 mice.
ICAM-1 和 LFA-1 抗体对乳品 DBA/1 小鼠 reo-2 触发的自身免疫性胰岛炎细胞因子 mRNA 表达的影响。
DOI: --
发表时间: 2003
期刊: J.Comp.Path.. 128
影响因子: --
作者: [Hayashi T, Hasegawa K, Morimoto M, Onodera T]
通讯作者: Onodera T
Elimination of CD4^+CD25^+T cell enhances Reo-2-triggered and CpG oligodeoxynucleotides-induced prolonged autoimmune insulitis in DBA/1J mice.
消除 CD4+CD25+T 细胞会增强 DBA/1J 小鼠中 Reo-2 触发的和 CpG 寡脱氧核苷酸诱导的长期自身免疫性胰岛炎。
DOI: --
发表时间: 2006
期刊: Scand.J.Immunol. 163
影响因子: --
作者: [Hayashi, T., Hasegawa, K., Sasaki, Y., Onodera, T.]
通讯作者: T.
DOI: 10.1111/j.0959-9673.2005.00438.x
发表时间: 2005-10-01
期刊: INTERNATIONAL JOURNAL OF EXPERIMENTAL PATHOLOGY
影响因子: 3
作者: [Hayashi, T, Hasegawa, K, Adachi, C]
通讯作者: Adachi, C
6
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