Fujigaki Y, Nagase M, Kojima K, Yamamoto T, Hishida A
First Department of Medicine, Hamamatsu University School of Medicine, Japan.
Virchows Arch. 1997 Jul;431(1):53-61. doi: 10.1007/s004280050069.
The ultrastructural localization of immune complex (IC) and inflammatory mediator systems in the glomerulus was investigated in active in situ IC glomerulonephritis employing cationized ferritin in rats. Glomerulonephritis was induced by unilateral renal perfusion of cationized ferritin as antigen (Ag) in preimmunized rats, and anti-ferritin antibody (Ab), C3 and the rat C5b-9 complex were localized by means of immunogold electron microscopy. Ag-Ab complexes were initially formed subendothelially, associated with C3, and attracted platelets, polymorphonuclear leucocytes (PMN) and monocytes. Then Ag-Ab complexes, without C3, passed across the glomerular basement membrane to re-aggregate subepithelially accompanied by C3 deposition after 1 day. Ag-Ab complexes without C3 accumulated in the inter-podocyte space within 1 day and were seen in the epithelial cells at 6 h. C5b-9 complexes were found in subepithelial immune deposits and in membrane vesicles of the epithelial cells, but only in very small amounts in subendothelial immune deposits. Accumulated platelets, PMN, and monocyte were in direct contact with endothelial cells or subendothelial IC. PMN and monocytes contained Ag, Ab and C3 in intracytoplasmic vacuoles. Ag-Ab complexes were also found in the mesangial matrix adjacent to the subendothelial region after 2 h and increased slightly in number, with expansion of the mesangial area thereafter. Most ICs formed in the subendothelial space rapidly formed lattices of a size that activated C3 and were then translocated to the subepithelial space. The potential ability of C3 to solubilize ICs in the subendothelial region may be important in this process. Endocytosis of subendothelial ICs by PMN and/or monocytes and the movement of ICs to the mesangial matrix may also contribute to the removal of IC from the subendothelial space.
采用阳离子铁蛋白，在大鼠原位免疫复合物性肾小球肾炎活动期研究肾小球中免疫复合物（IC）和炎症介质系统的超微结构定位。通过对预先免疫的大鼠单侧肾脏灌注阳离子铁蛋白作为抗原（Ag）诱导肾小球肾炎，采用免疫金电子显微镜对抗铁蛋白抗体（Ab）、C3和大鼠C5b - 9复合物进行定位。Ag - Ab复合物最初在内皮下形成，与C3相关，并吸引血小板、多形核白细胞（PMN）和单核细胞。然后，不含C3的Ag - Ab复合物穿过肾小球基底膜，在1天后重新在上皮下聚集并伴有C3沉积。不含C3的Ag - Ab复合物在1天内积聚在足细胞间间隙，并在6小时时出现在上皮细胞中。C5b - 9复合物见于上皮下免疫沉积物和上皮细胞膜囊泡中，但在内皮下免疫沉积物中含量极少。积聚的血小板、PMN和单核细胞与内皮细胞或内皮下IC直接接触。PMN和单核细胞的胞质空泡中含有Ag、Ab和C3。2小时后，在内皮下区域相邻的系膜基质中也发现了Ag - Ab复合物，其数量略有增加，此后系膜区域扩大。大多数在内皮下空间形成的IC迅速形成激活C3的大小的晶格，然后转移到上皮下空间。C3在内皮下区域溶解IC的潜在能力在此过程中可能很重要。PMN和/或单核细胞对内皮下IC的内吞作用以及IC向系膜基质的移动也可能有助于从内皮下空间清除IC。
