In situ immune complex nephritis using cationic antigens - mediator system involved in the glomerular injury -
使用阳离子抗原的原位免疫复合物肾炎 - 参与肾小球损伤的介质系统 -
基本信息
- 批准号:60570153
- 负责人:
- 金额:$ 1.22万
- 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:1985
- 资助国家:日本
- 起止时间:1985 至 1986
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
With aid of the above grant, we have studied and reported on an in situ immune complex (IC) nephritis using cationic antigens. The following results have been obtained: During the former period of project,1. Cationized ferritin, electronmicroscopically visible antigen, was able to induce in situ IC nephritis as well as cationized human IgG.2. The initial site of in situ IC formation occured mainly on the subendothelial side of glomerular basement membrane (GBM).3. The local IC formation was followed by the accumulation of blood-born cells, such as polymorphonuclear leukocyte (PMN) and monocyte.4. Proteinuria was abolished in three mediator-depleted groups (C3, PMN or monocyte depleted). In the latter half of the period,5. SDS-polyacrylamide gel electrophoresis analysis of urinary protein revelaed a urinary leak of high molecular weight proteins (MW. 145 and 200 Kds) in our model, as well as in Masugi nephritis.6. Using culture of isolated glomeruli, interleukin 1-like substance, probably produced by mesangial cells, was detected in culture medium. Furthermore, we found a monocyte-derived factor which was able to induce proliferation of mesangial cells in vitro.
在上述资助的帮助下,我们研究并报道了使用阳离子抗原的原位免疫复合物(IC)肾炎。取得了以下成果:项目前期,1.阳离子化铁蛋白是电镜下可见的抗原,与阳离子化人IgG一样能诱导原位IC肾炎。原位IC形成的起始部位主要位于肾小球基底膜(GBM)的内皮下侧.局部IC的形成伴随着血生细胞的聚集,如多形核白细胞(PMN)和单核细胞.蛋白尿在三个介质去除组(C3,PMN或单核细胞去除)中被消除。后半期,5.尿蛋白SDS-聚丙烯酰胺凝胶电泳分析显示尿中有高分子量蛋白(MW)渗漏。145和200 Kds),以及在Masugi肾炎。利用离体肾小球培养,在培养液中检测到可能由系膜细胞产生的白细胞介素1样物质。此外,我们发现了一种单核细胞衍生因子,它能够在体外诱导系膜细胞增殖。
项目成果
期刊论文数量(37)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Nakamura, Takamichi: "Hito jinsikyuutai seibun ni taisuru monokuronaru koutai" Niigata igakukai zatsusi. 100. 316-322 (1986)
中村高道:“Hito jinsikyuutai seibun ni taisuru monokuronaru koutai”Niigata igakukai zatsusi。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
Oite, Takashi: "Ultramicroscopic localization of cationized antigen in the glomerular basement membrane in the course of active, in situ immune complex glomerulonephritis." Virchows Arch [Cell Pathol]. 48. 108-118 (1985)
Oite, Takashi:“在活跃的原位免疫复合物肾小球肾炎过程中,阳离子化抗原在肾小球基底膜中的超显微定位。”
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
Oite, Takashi: "Masugi jinen kara in situ immune complex jinen" Jin to Toseki. 22. 259-263 (1987)
大手隆:“Masugi jinen kara 原位免疫复合物 jinen” Jin to Toseki。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
Kimura, Satoshi: "Monoclonal autoantibodies in Heymann nephritis." Clin.exp.Immunol.64. 28-33 (1986)
Kimura, Satoshi:“海曼肾炎的单克隆自身抗体。”
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
Oite,Takashi: Virchows Arch[cell Pathol]. 48. 108-118 (1985)
Oite,Takashi:Virchows Arch[细胞病理]。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
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OITE Takashi其他文献
OITE Takashi的其他文献
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{{ truncateString('OITE Takashi', 18)}}的其他基金
Functional analysis of mesangial cell syncytium and elucidation of mechanisms involving progressive glomerulosclerosis
系膜细胞合胞体的功能分析和进展性肾小球硬化机制的阐明
- 批准号:
15390266 - 财政年份:2003
- 资助金额:
$ 1.22万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
Identification of the molecular epitope associated with mesangical cell function.
与系膜细胞功能相关的分子表位的鉴定。
- 批准号:
08670241 - 财政年份:1996
- 资助金额:
$ 1.22万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Regulation loss of mesangial cell function leading to irreversible, glomerular sclerosis.
系膜细胞功能调节丧失导致不可逆的肾小球硬化。
- 批准号:
06670215 - 财政年份:1994
- 资助金额:
$ 1.22万 - 项目类别:
Grant-in-Aid for General Scientific Research (C)
Mechanisms of sclerosis in the glomerulus as a representative of microcirculation
作为微循环代表的肾小球硬化机制
- 批准号:
04670199 - 财政年份:1992
- 资助金额:
$ 1.22万 - 项目类别:
Grant-in-Aid for General Scientific Research (C)
Mechanisms of cell proliferation and extracellular matrix production in glomeruli
肾小球细胞增殖和细胞外基质产生的机制
- 批准号:
63570155 - 财政年份:1988
- 资助金额:
$ 1.22万 - 项目类别:
Grant-in-Aid for General Scientific Research (C)