摘要
从正常大鼠肾小管刷状缘微绒毛上提取致病的小管抗原(Tub-Ag)免疫白兔可获得相应的抗血清。给大鼠被动注射此种抗血清后5分钟荧光检测即可见鼠肾小球毛细血管壁上出现兔抗体IgG。约1周后,实验鼠便产生了典型的膜性肾炎样的临床及病理学改变。应用小管抗体(Tub-Ab)进行鼠肾动脉灌注实验,结果表明:在缺乏CIC的情况下,灌注的抗体能与GBM上皮侧、裂隙孔等处结合,IC出现的部位与PHN大鼠IC的位置基本相似。上述实验均提示:PHN的发病机制乃是Tub-Ab与肾小球中固定的抗原直接结合,进而导致上皮下IC原位形成。
The corresponding antiserum was acquired by immunizing rabbits with the nephritogenic tubular epithelial antigen (Tub-Ag) isolated from renal tubular brush border microvillus membranes of normal rats. 5 minutes after the passive injection into rats with the antiserum, the rabbits antibody IgG along the glomerular capillary walls of the rats was found by immunofluorescence.About one week,the rats induced typical clinicopathologic changes resembling that of human membranous nephritis. Moreover, the purified antibody against nephritogenic Tub-Ag was perfused into rat renal artery. And the results indicate that the perfused antibody can bind to epithelial side of GBM and filtration slit membrane in absence of CIC; the locations of glomerular IC in perfusion are similar to those of glomerular IC in PHN. These experiments suggested that the pathogenesis of PHN is the binding of the Tub-Ab to fixed Tub-Ag present in the glomeruli, which contributes to in situ formation of subepithelial immune complexes.
出处
《免疫学杂志》
CAS
CSCD
北大核心
1990年第4期247-251,共5页
Immunological Journal
关键词
肾炎
HN
模型
发病机制
Passive Heymann nephritis, Perfusion of rat renal artery, Insitu formation of IC
