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首页> 外文期刊>Clinical immunology: The official journal of the Clinical Immunology Society >C3 is central to the interstitial component of experimental immune complex glomerulonephritis.
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C3 is central to the interstitial component of experimental immune complex glomerulonephritis.

机译：C3对于实验性免疫复合物肾小球肾炎的间质成分至关重要。

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摘要

We have suggested that renal tubular synthesis of C3 and its activation in the cortical interstitium is a mechanism for the progression of glomerulonephritis to interstitial injury. To test this hypothesis, immune complex glomerulonephritis was induced in C57BL/6 mice by intraperitoneal injections of horse spleen apoferritin and lipopolysaccharide (HSA/LPS). When compared to wild-type (WT) animals, C3 knockout (C3KO) mice had glomerular changes that were identical. Morphometric analysis of the cortical interstitium, however, showed marked differences. WT mice had more interstitial inflammation, edema, and tubular atrophy, when compared to C3KO mice. At the end of the experiment, WT animals also had significantly more proteinuria than did C3KOs. These experiments provide further evidence of a role of locally synthesized complement in the progression of glomerular disease.
机译：我们已经提出，C3的肾小管合成及其在皮层间质中的激活是肾小球肾炎发展为间质性损伤的机制。为了验证这一假设，通过腹膜内注射马脾载铁蛋白和脂多糖（HSA / LPS）在C57BL / 6小鼠中诱发了免疫复合物肾小球肾炎。与野生型（WT）动物相比，C3基因敲除（C3KO）小鼠的肾小球变化是相同的。然而，皮质间质的形态计量学分析显示出明显的差异。与C3KO小鼠相比，WT小鼠具有更多的组织间炎症，水肿和肾小管萎缩。在实验结束时，野生型动物的蛋白尿也比C3KO多得多。这些实验提供了进一步证明局部合成的补体在肾小球疾病进展中的作用。

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