Fate of immune complexes, glomerulonephritis, and cell-mediated vasculitis in lupus-prone MRL/Mp lpr/lpr mice
Fate of immune complexes, glomerulonephritis, and cell-mediated vasculitis in lupus-prone MRL/Mp lpr/lpr mice
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DOI：
10.1006/exmp.2000.2330
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发表时间：
2000-12-01
影响因子：
3.6
通讯作者：
Dilioglou, S
中科院分区：
文献类型：
--
作者：
Cruse, JM;Lewis, RE;Dilioglou, S
通过将I-125-BSA注射到雌性MRL/Mp lpr/lpr小鼠和MRL/Mp +/+小鼠中诱导免疫复合物形成，所述雌性MRL/Mp lpr/lpr小鼠发展自发性系统性红斑狼疮（SLE）样疾病，所述雌性MRL/Mp +/+小鼠不发展自发性系统性红斑狼疮（SLE）样疾病。在指定的时间间隔后，注射10毫克的I-125-牛血清白蛋白（BSA），非狼疮小鼠发展稀疏，小的电子致密沉积物在系膜区和上皮下免疫沉积物进行部分解决。相比之下，SLE易感小鼠肾脏的肾小球显示系膜细胞增殖和系膜基质物质的一些增加。存在大量上皮下和系膜区电子致密沉积物。还发现了一些内皮下和膜内沉积物。毛细血管腔中含有大量的电子致密沉积物。观察到的正在消退的上皮下沉积物不到非SLE小鼠肾脏中发现的数量的一半。在注射I-125-BSA后，每天还记录全身计数。然而，到接种后第12天，狼疮易感小鼠和非SLE对照小鼠均以相同的速率消除I-125-BSA，而患有SLE样疾病的小鼠在第6天至第12天之间I-125-BSA消除率下降。结果表明，SLE易感小鼠分解免疫复合物的能力受损，无论它们是核-抗核的还是来自外源的，即，BSA-抗-BSA，在此外源性免疫复合物形成对系统性红斑狼疮样疾病的叠加的实验模型中与对照相比。(C)北京大学出版社.
Immune complex formation was induced by the injection of I-125-BSA into female MRL/Mp lpr/lpr mice, which develop spontaneous systemic lupus erythematosus (SLE)-like disease, and MRL/Mp +/+ mice, which do not. At designated intervals following the injection of 10 mg of I-125-bovine serum albumin (BSA), the nonlupus mice developed sparse, small electron-dense deposits in mesangial areas and subepithelial immune deposits that underwent partial resolution. By contrast, glomeruli of the SLE-prone mouse kidneys revealed proliferation of mesangial cells and some increase in mesangial matrix material. Numerous subepithelial and mesangial electron-dense deposits were present. Some subendothelial and intramembranous deposits were also demonstrated. Capillary lumens contained massive electron-dense deposits. The resolving subepithelial deposits observed were fewer than half the number found in kidneys of the non-SLE mice. Whole body counts were also recorded daily following the injection of I-125-BSA. Whereas, both lupus-prone and non-SLE control mice eliminated I-125-BSA at equivalent rates through day 12 postinoculation, those with SLE-like disease showed a decreased I-125-BSA elimination rate between days 6 and 12. Results suggest an impairment in the ability of SLE-prone mice to resolve immune complexes, whether they are nuclear-antinuclear or from an exogenous source, i.e., BSA-anti-BSA, compared to controls in this experimental model of the superimposition of exogenous immune complex formation on systemic lupus erythematosus-like disease. (C) 2000 Academic Press.