Rantala I
Nephron. 1981;29(5-6):239-44. doi: 10.1159/000182381.
Autologous immune complex-type nephritis was induced in Sprague-Dawley rats. The animals were killed when daily urinary protein excretion exceeded 300 mg (group 1) or 70-100 mg (group 2). Normal rats served as controls (group 3). Endocytosis of immune deposits by glomerular visceral epithelial cells was investigated by conventional and immunoelectron microscopy. In group 1, membranous glomerulonephritis was confirmed by conventional electron microscopy and immunofluorescence microscopy. By the former technique abundant endocytotic activity was shown in epithelial cells and by immunoelectron microscopy rat IgG was demonstrated in both the deposits and the epithelial cell phagosomes. Groups 2 and 3 were very similar and the presence of IgG could not be demonstrated. Results from group 1 strongly support the assumption that at least part of the phagosomes are derived from the deposits. Endocytosis seems to be dependent on the degree of membrane damage and the amount of immune deposits.
在斯普拉格-道利大鼠中诱发自体免疫复合物型肾炎。当每日尿蛋白排泄量超过300毫克（第1组）或70 - 100毫克（第2组）时，处死动物。正常大鼠作为对照（第3组）。通过传统和免疫电子显微镜研究肾小球脏层上皮细胞对免疫沉积物的内吞作用。在第1组中，通过传统电子显微镜和免疫荧光显微镜证实为膜性肾小球肾炎。通过前一种技术显示上皮细胞中有丰富的内吞活性，通过免疫电子显微镜在沉积物和上皮细胞吞噬体中均证实有大鼠IgG。第2组和第3组非常相似，未证实有IgG存在。第1组的结果有力地支持了至少部分吞噬体来源于沉积物这一假设。内吞作用似乎取决于膜损伤程度和免疫沉积物的量。
