Immunopathologic Study on The Pathogenesis of Glomerulonephritis

该项目的目的是研究免疫肾小球损伤的机制，特别是研究抗体与植入肾小球内皮（GEN）的抗原相互作用后的事件。为此，通过离体肾灌注技术将凝集素植入GEN，然后对灌注后的肾脏进行再血管化。急性肾小球肾炎是由静脉注射抗凝集素抗体引起的。在HPA的情况下，抗体给药后，通过涉及细胞骨架的补丁/脱落机制，在GEN上立即形成颗粒状的HPA-anti-HPA免疫沉积物（id）。这些IDs从肾小球毛细血管壁的管腔方向移动到上皮下区域，表明在该模型中膜样病变是可诱导的。此外，还从大鼠肾小球细胞的质膜中纯化了hpa结合糖蛋白。兔对该蛋白的抗体与足细胞的自由表面特异性反应，其表位的性质被认为与了解某种人类肾小球肾炎有关。

The aim of the project was to study the mechanisms of immune glomerular injury, particularly to study the events following the interaction of antibodies with antigen planted on the glomerular endothelium (GEN). For this purpose, a lectin was implanted on the GEN by isolated kidney perfusion technique and subsequent re-vascularization of perfused kidney. Acute glomerulonephritis was induced by the intravenous administration of anti-lectin antibodies. In case of HPA, granular HPA-anti-HPA immune deposits (IDs) were formed on the GEN immediately after antibody administration possively through the mechanisms of patching/shedding involving cytoskeleton. These IDs moved from the luminal aspect of the glomerular capillary wall to the subepithelial area suggesting that membranous-like lesion was inducible in this model. In addition, HPA-binding glycoprotein was purified from the plasma membrane of rat glomerular cells. Rabbit antibodies to this protein reacted specifically with the free surface of podocytes and the nature of the epitope(s) was thought to be pertinent to the understanding of some kind of human glomerulonephritis.