Batsford S R, Takamiya M, Vogt A
Clin Nephrol. 1980 Nov;14(5):211-6.
In the model described here the ability of cationized (basic) ferritin to bind to the glomerular basement membrane and act as a planted antigen was exploited. This planted antigen was accessible to circulating antibody resulting in in situ immune complex formation. Perfusion of cationized ferritin (isoelectric point greater than 9.5) directly into the renal arteries, followed by intravenous injection of anti-ferritin antibody resulted in induction of glomerulonephritis with heavy proteinuria lasting for about 3 weeks. Fine granular deposition of antigen, antibody and rat C3 along the glomerular capillary walls was seen by immunofluorescence. Electron microscopy revealed the presence of subepithelial deposits containing ferritin; the foot processes were fused. This demonstrates the potential role of basic antigens in the pathogenesis of in situ immune complex glomerulonephritis.
在此描述的模型中，利用了阳离子化（碱性）铁蛋白结合肾小球基底膜并作为植入抗原的能力。这种植入抗原可被循环抗体识别，从而导致原位免疫复合物形成。将阳离子化铁蛋白（等电点大于9.5）直接灌注到肾动脉中，随后静脉注射抗铁蛋白抗体，可诱导出伴有重度蛋白尿的肾小球肾炎，持续约3周。通过免疫荧光可见抗原、抗体和大鼠C3沿肾小球毛细血管壁呈细颗粒状沉积。电子显微镜检查显示存在含有铁蛋白的上皮下沉积物；足突融合。这证明了碱性抗原在原位免疫复合物性肾小球肾炎发病机制中的潜在作用。
