Kerjaschki D
Verh Dtsch Ges Pathol. 1989;73:24-35.
Glomerular subepithelial immune deposits are the hallmark of human membranous glomerulopathy, and of its corresponding experimental rat model, Heymann nephritis (HN). The pathogenesis of HN is now understood in some detail, and recent data on this issue are reviewed in this summary. Immune deposits in HN are caused by the interaction of certain epitopes on the nephritogenic antigen, the glycoprotein gp 330, which is a resident molecule of the clathrin coated pits of glomerular visceral epithelial cells, and specific anti-gp 330 IgG. This step is followed within minutes by detachment of the immune complexes and rapid and firm cross-linking to the glomerular basement membrane, thus preventing its endocytosis by the epithelial cells. Immune complexes accumulate locally to form large immune deposits by repeated cycles of antibody binding to newly synthetized gp 330 antigen, shedding and immobilization in the basement membrane. Also human kidneys contain a gp 330-related (but not identical) protein which appears to be not involved in the formation of immune deposits. However, recent data suggest that also in the human disease similar pathogenic mechanisms as in HN could be involved.
肾小球上皮下免疫沉积物是人类膜性肾小球病及其相应的实验大鼠模型——海曼肾炎（HN）的标志。目前对HN的发病机制已有一定程度的了解，本综述将对此问题的最新数据进行回顾。HN中的免疫沉积物是由致肾炎抗原（糖蛋白gp 330，它是肾小球脏层上皮细胞网格蛋白包被小窝的固有分子）上的某些表位与特异性抗gp 330 IgG相互作用引起的。在这一步骤之后，几分钟内免疫复合物就会脱离，并迅速牢固地交联到肾小球基底膜上，从而阻止其被上皮细胞内吞。免疫复合物通过抗体与新合成的gp 330抗原反复结合、脱落并固定在基底膜上的循环过程，在局部积累形成大的免疫沉积物。此外，人类肾脏含有一种与gp 330相关（但不相同）的蛋白质，它似乎不参与免疫沉积物的形成。然而，最近的数据表明，人类疾病中可能也涉及与HN类似的致病机制。
