In situ immune complex nephritis using cationic antigens - mediator system involved in the glomerular injury -

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。

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.