Hurd E R, Ziff M
Clin Exp Immunol. 1977 Feb;27(2):261-8.
Using the NZB and NZB/NZW F1 (B/W) hybrid mouse as a model for systemic lupus erythematosus, an effort has been made to quantitate: (1) immune complex deposition in the glomeruli by immunofluorescent staining of immunoglobulin, (2) glomerular cellular proliferation by radioautographic measurement of [3H]Tdr incorporation into the glomerular cells in vivo, and (3) glomerular scarring by PAS staining. The relationship between these changes and increasing age has been examined. By radioautography it was observed that dividing glomerular cells were labelled in vivo after injection of [3H]Tdr. This provided a reproducible measure of the proliferative process in the nephritis of B/W mice. In C57B1/6J and CBA/J mice, which have a low incidence of glomerular disease, little change in the amount of glomerular cell proliferation was observed with increasing age. The NZB strain of animals showed a somewhat increased level of proliferation but this did not increase with age. In striking contrast, glomerular cell proliferation in the B/W mice increased rapidly with age. The earliest change observed in the kidney was the deposition of immunofluorescent material in the mesangium and glomerular capillary basement membrane beginning between 3 and 5 months of age and reaching a peak at 9 months. Increase in glomerular cell proliferation began about 2 months after the onset of immune complex deposition but also reached a maximum at 7 months. Glomerular sclerosis was the last change to appear and continued after the other two parameters measured has begun to decline. These data suggest that the deposition of immune complexes in the glomerulus may be an important triggering mechanism for renal cell proliferation and glomerulosclerosis in the B/W mouse. The techniques described would provide a sensitive and reproducible quantitative method for analysing the differential effects of various types of treatment of immune complex nephritis in animals.
以新西兰黑鼠（NZB）和新西兰黑鼠/新西兰白鼠F1（B/W）杂交小鼠作为系统性红斑狼疮的模型，已开展了以下定量研究：（1）通过免疫球蛋白免疫荧光染色对肾小球内免疫复合物沉积进行定量；（2）通过放射自显影测量体内[3H]胸腺嘧啶核苷（[3H]Tdr）掺入肾小球细胞的情况对肾小球细胞增殖进行定量；（3）通过过碘酸雪夫（PAS）染色对肾小球瘢痕形成进行定量。已研究了这些变化与年龄增长之间的关系。通过放射自显影观察到，注射[3H]Tdr后，体内分裂的肾小球细胞被标记。这为B/W小鼠肾炎中的增殖过程提供了一种可重复的测量方法。在肾小球疾病发病率较低的C57B1/6J和CBA/J小鼠中，随着年龄增长，肾小球细胞增殖量几乎没有变化。NZB品系动物的增殖水平有所升高，但未随年龄增加。与之形成鲜明对比的是，B/W小鼠的肾小球细胞增殖随年龄迅速增加。在肾脏中最早观察到的变化是免疫荧光物质在系膜和肾小球毛细血管基底膜沉积，始于3至5月龄之间，并在9月龄达到峰值。肾小球细胞增殖增加始于免疫复合物沉积开始约2个月后，但也在7月龄达到最大值。肾小球硬化是最后出现的变化，在其他两个测量参数开始下降后仍持续存在。这些数据表明，肾小球内免疫复合物的沉积可能是B/W小鼠肾细胞增殖和肾小球硬化的重要触发机制。所描述的技术将为分析动物免疫复合物性肾炎各种治疗方法的不同效果提供一种灵敏且可重复的定量方法。
