Rifai A, Small P A, Teague P O, Ayoub E M
J Exp Med. 1979 Nov 1;150(5):1161-73. doi: 10.1084/jem.150.5.1161.
An animal model for IgA immune complex nephritis was developed. IgA immune complexes formed in vitro with an IgA anti-dinitrophenyl (DNP) derived from MOPC-315 plasmacytoma, and dinitrophenylated bovine serum albumin (DNP-BSA) produced mild focal glomerulonephritis in mice. Similar, but more severe pathological changes were produced with complexes formed in vivo either in normal mice or MOPC-315 tumor-bearing mice. In contrast to the focal nature of the PAS-positive glomerular lesions observed by light microscopy, immunofluorescent examination revealed IgA deposits in all glomeruli. This discrepancy between immunofluorescent and histopathologic findings as well as the distribution of the immune complexes within the affected glomeruli, are some of the features which bear resemblance between this experimental model and human IgA nephropathy. Fixation of complements by DNP-BSA-IgA immune complexes, formed in vitro or in vivo, was shown to occur in the glomeruli of mice with IgA immune complex nephropathy. The pattern of C3 glomerular deposits was similar to that of IgA. However, complement proved to be nonessential for complex deposition. This conclusion is based on the observation that decomplemented mice, although showing no deposition of C3 in their glomerulus, developed glomerular immunohistological changes similar to those observed in experimental mice that were not decomplemented. Polymeric IgA was observed to be critical for renal deposition of complexes and induction of nephritic histological changes. In contrast, monomeric IgA immune complexes failed to produce glomerular deposits. This finding raises the possibility that secretory IgA, which is predominantly polymeric, may play a role in human IgA-associated glomerulonephritis.
建立了IgA免疫复合物性肾炎的动物模型。用源自MOPC - 315浆细胞瘤的IgA抗二硝基苯基（DNP）与二硝基苯基化牛血清白蛋白（DNP - BSA）在体外形成的IgA免疫复合物，可在小鼠中引起轻度局灶性肾小球肾炎。在正常小鼠或携带MOPC - 315肿瘤的小鼠体内形成的复合物也会产生类似但更严重的病理变化。与光镜下观察到的PAS阳性肾小球病变的局灶性性质相反，免疫荧光检查显示所有肾小球均有IgA沉积。免疫荧光和组织病理学结果之间的这种差异以及免疫复合物在受影响肾小球内的分布，是该实验模型与人类IgA肾病相似的一些特征。体外或体内形成的DNP - BSA - IgA免疫复合物在IgA免疫复合物性肾炎小鼠的肾小球中可发生补体固定。C3肾小球沉积物的模式与IgA相似。然而，补体被证明对复合物沉积并非必需。这一结论基于以下观察结果：去补体小鼠虽然肾小球中未显示C3沉积，但出现了与未去补体的实验小鼠相似的肾小球免疫组织学变化。观察到聚合IgA对复合物的肾脏沉积和肾炎组织学变化的诱导至关重要。相比之下，单体IgA免疫复合物未能产生肾小球沉积物。这一发现增加了主要为聚合形式的分泌型IgA可能在人类IgA相关肾小球肾炎中起作用的可能性。
