Experimental IgA nephropathy
Experimental IgA nephropathy
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实验性 IgA 肾病
DOI：
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发表时间：
1979
影响因子：
15.3
通讯作者：
E. Ayoub
中科院分区：
文献类型：
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作者：
A. Rifai;P. Small;P. Teague;E. Ayoub
建立了IgA免疫复合体肾炎的动物模型。用MOPC-315浆细胞瘤免疫球蛋白(DNP)和二硝基苯化牛血清白蛋白(DNP-BSA)在体外形成免疫复合物，造成小鼠轻度局灶性肾小球肾炎。无论是正常小鼠还是MOPC-315荷瘤小鼠，体内形成的复合体都会产生类似的、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不同，免疫荧光检查显示所有肾小球内均有IgA沉积。免疫荧光和组织病理学结果之间的差异以及免疫复合体在受影响的肾小球内的分布，是该实验模型与人类IgA肾病之间的一些相似之处。在体外或体内形成的DNP-BSA-IgA免疫复合体对补体的固定作用发生在IgA免疫复合体肾病小鼠的肾小球中。C3肾小球沉积模式与IgA相似。然而，补体被证明不是复杂沉积所必需的。这一结论是基于观察到，尽管去补体小鼠的肾小球中没有C3沉积，但发生了与未去补小鼠实验小鼠相似的肾小球免疫组织学变化。聚合的IgA被观察到是肾脏复合体沉积和诱导肾炎组织学改变的关键。相比之下，单体IgA免疫复合体不能产生肾小球沉积。这一发现提出了一种可能性，即分泌型IgA可能在人类IgA相关性肾炎中发挥作用。
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.