| Budget Amount *help |
¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 1986: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1985: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Research Abstract |
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.
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