Fleuren G J, vd Lee R, Greben H A, Van Damme B J, Hoedemaeker P J
Lab Invest. 1978 Apr;38(4):496-501.
Heterologous immune complex glomerulonephritis can be induced in various strains of rats by one injection of heterologous antibody directed against antigens present in the brush border of the proximal. Although it is generally believed that an immune complex glomerulonephritis is caused by the deposition of soluble immune complexes from the circulation in the glomerular basement membrane, there are reasons for doubting whether this mechanism is also operating in the type of experimental glomerulonephritis presented here. In a study using injections of extra antibody and extra antigen to influence the formation and deposition of immune complexes, it is demonstrated that this type of glomerulonephritis is induced in a state of antibody excess. The theory that only immune complexes formed in antigen excess can deposit in the glomerular basement membrane, warrants the assumption that in our model a different pathogenetic mechanism is operating. The hypothesis is put forward that in the heterologous immune complex glomerulonephritis free antibody crosses the glomerular basement membrane to combine with the antigen. This antigen either crosses the glomerular basement membrane separately or is already present as an integral part of this structure.
通过单次注射针对近端肾小管刷状缘存在的抗原的异源抗体，可在多种品系的大鼠中诱发异源免疫复合物肾小球肾炎。尽管人们普遍认为免疫复合物肾小球肾炎是由循环中的可溶性免疫复合物沉积于肾小球基底膜所致，但有理由怀疑在此处呈现的实验性肾小球肾炎类型中该机制是否也起作用。在一项使用注射额外抗体和额外抗原以影响免疫复合物形成和沉积的研究中，证明这种类型的肾小球肾炎是在抗体过量的状态下诱发的。只有在抗原过量时形成的免疫复合物才能沉积于肾小球基底膜的理论，使得我们假设在我们的模型中存在不同的致病机制。有人提出假说，在异源免疫复合物肾小球肾炎中，游离抗体穿过肾小球基底膜与抗原结合。这种抗原要么单独穿过肾小球基底膜，要么已经作为该结构的一个组成部分存在。
