Boonpucknavig V, Boonpucknavig S, Bhamarapravati N
Am J Pathol. 1973 Jan;70(1):89-108.
Renal glomeruli of Plasmodium berghei infected mice were studied electron microscopically. The endothelial cell proliferation and endothelial cytoplasmic changes were greatly stimulated on day 7, at the time when there were collections of dense granular aggregates in the glomerular capillary lumens and electron-dense deposits in the mesangial areas. The basement membrane lesion developed with the infiltration of polymorphonuclear leucocytes on day 14 with more electron-dense deposits in the mesangial areas and in the basement membrane. On the basis of these ultrastructural alterations and on previous findings of immune complex (P berghei antigen, mouse globulin and mouse beta1C globulin) deposits by immunofluorescent study, we concluded that glomerular lesions in P berghei infected mice are induced by immune mechanism.
用电子显微镜研究了感染伯氏疟原虫小鼠的肾小球。在第7天，当肾小球毛细血管腔内有密集的颗粒聚集体以及系膜区有电子致密沉积物时，内皮细胞增殖和内皮细胞质变化受到极大刺激。在第14天，随着多形核白细胞浸润，基底膜病变出现，系膜区和基底膜中有更多电子致密沉积物。基于这些超微结构改变以及免疫荧光研究先前发现的免疫复合物（伯氏疟原虫抗原、小鼠球蛋白和小鼠β1C球蛋白）沉积，我们得出结论，感染伯氏疟原虫小鼠的肾小球病变是由免疫机制诱导的。
