Hunsicker L G, Shearer T P, Plattner S B, Weisenburger D
J Exp Med. 1979 Sep 19;150(3):413-25. doi: 10.1084/jem.150.3.413.
We have investigated the pathogenesis of glomerular hypercellularity seen in acute serum sickness nephritis induced in rabbits with bovine serum albumin (BSA). The increase in cellularity began with the first stages of immune clearance of BSA, with a peak cellularity occuring at the time of onset of proteinuria. Although there was a significant increase in the fraction of glomerular cells incorporating [3H]thymidine, first seen at the onset of proteinuria, this increase occurred too late and was too small to explain the observed rate of increase in glomerular cellularity. On the other hand, a striking monocytic infiltration of the glomeruli was documented by electron microscopy and by staining for nonspecific esterase. This monocytic infiltration paralleled the observed course of glomerular hypercellularity and was quantitatively sufficient to explain the total increase seen. It appears, therefore, that glomerular hypercellularity seen in this model is principally a result of monocyte infiltration.
我们研究了用牛血清白蛋白（BSA）诱导的兔急性血清病肾炎中所见的肾小球细胞增多症的发病机制。细胞增多始于BSA免疫清除的最初阶段，蛋白尿开始时细胞增多达到峰值。尽管在蛋白尿开始时首次观察到掺入[3H]胸腺嘧啶核苷的肾小球细胞比例显著增加，但这种增加出现得太晚且太小，无法解释观察到的肾小球细胞增多率。另一方面，通过电子显微镜和非特异性酯酶染色记录到肾小球有明显的单核细胞浸润。这种单核细胞浸润与观察到的肾小球细胞增多过程平行，在数量上足以解释所见的总体增加。因此，在该模型中所见的肾小球细胞增多主要是单核细胞浸润的结果。
