Basic study on prevention and treatment of type 1 diabetes mellitus with biological respomse modifiers.
Basic study on prevention and treatment of type 1 diabetes mellitus with biological respomse modifiers.
批准号:
61570536
负责人:
SATOH Jo
金额:
$1.34万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for General Scientific Research (C)
财政年份:
1986
资助国家:
日本
项目状态:
已结题
起止时间:
1986 至 1987
中文摘要
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英文摘要
We previously reported that a streptococcal preparation (OK-432), one of BRMs, inhibited insulitis and prevented insulin-dependent (type 1) diabetes mellitus (IDDM) in NOD mice. In this project, we extended our previous observation to two studies; 1) effect of OK-432 on IDDM in BB rats as an another model of IDDM and 2) analysis of mechanisms of OK-432-action by usingNOD mice. The results and conslusions are as follows.1)The cumulative incidence of diabetes was 27.7% (13/47) by 30 weeks of age in BB rats, whereas that was significantly suppressed in the rats (7.4%, 4/54, p<0.01) who were weekly and intraperitoneally treated with 0.2 mg of OK-432. Histological examinations revealed that the OK-432-treated BB rats retained a greater number of intact islets without lymphocytic infiltrations than did thenon-treated rats. The cytotoxic activities of spleen cells directed against a rat insulinoma cell line, RIN, were significantly suppressed in the OK-432-treated BB rats as compared with tho … More se in the non-treated rats, Thus, the OK-432 treatment suppressed insulitis and inhibited development of diabetes not only in NOD mice but also in BB rats.2) Approximately 85% of the non-treated NOD mice developed diabetes by 25 weeks of age. On the other hand, the weekly injection (ip or iv) of 0.1mg of OK-432 from 4 or 5 to 15 ro 20 weeks of age completely inhibited development of diabetes and these NOD mice did not develop diabetes even after ceasing the OK-432-treatment. Cyclophosphamide enhanced the development of diabetes in thenon-treated NOD mice but not in the OK-432-treated mice. The diabetes wastransfered by the spleen cells from the non-treated NOD mice but not by the cells from the OK-432-treated mice. In addition, the spleen cells from the OK-432-treated mice inhibited the development of diabetes in the cyclophosphamide-treated mice and this inhibitory effect was eliminated by the treatment of cells with anti-Thy-1 antibody and complement. These indicate that the OK-432-treatment inhibited the induction of cytotoxic effector cells directed against pancreatic B cells and this effect was mediated by suppressor T cells. Less
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新谷茂樹,他: 糖尿病動物. (1987)
Shigeki Shintani 等人:糖尿病动物(1987)。
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Jo Satoh et al: "NOD/Sendai mice with high incidence of type 1 diabetes are not T lymphocytopenic" in submission.
Jo Satoh 等人提交的文章中称:“1 型糖尿病发病率高的 NOD/Sendai 小鼠并非 T 淋巴细胞减少症”。
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佐藤譲,他: 日本内科学会雑誌. 76. 124 (1987)
Yuzuru Sato 等人:日本内科学会杂志 76. 124 (1987)。
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後藤由夫,佐藤譲他編: "糖尿病動物1・OK-432によるBBラット糖尿病発症の抑制" 医療ジャーナル社, 101-107 (1987)
Yoshio Goto、Yuzuru Sato 等编:“糖尿病动物 1 和 OK-432 对 BB 大鼠糖尿病发病的抑制”医学杂志出版,101-107 (1987)
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新谷茂樹,他: 日本免疫学会総会・学術集会記録. 16. 678 (1986)
Shigeki Shintani 等:日本免疫学会会员大会和学术会议记录 16. 678 (1986)。
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共 6 条
Screening of clinical medicines for effects on gene expressions and protein productions of adipocytokines by using a newly-isolated preadipocyte line
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Study on associations of novel TNF-α promoter polymorphisms with diabetes and diabetic complications
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Expression of UCP-2 and UCP-3 genes in obese type 2 diabetes mellitus and its modification by a cytokine inducer
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Abnomal cytokine expression in diabetes mellitus and diabetic complications, and their treatment by cytokine control
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财政年份:1994
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Study on mechanism of action of biological response modifier (BRM) in prevention of type 1 diabetes mellitus.
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批准号:63570520
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资助金额:$1.28万
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财政年份:1988
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依托单位:
Screening of biological response modifiers (BRMs) for preventive effects on type 1 diabetes mellitus in animal models.
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批准号:62870046
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项目类别:Grant-in-Aid for Developmental Scientific Research
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资助金额:$2.43万
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财政年份:1987
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负责人:SATOH Jo
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依托单位:
国内基金
海外基金
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GRP78保护胰岛β细胞与重建IDDM免疫耐受效应与机制研究
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预防和治疗胰岛素依赖型糖尿病(IDDM)的新方法- - 利用ILA微小肽段诱导针对自身胰岛抗原免疫耐受的研究
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