Barabas A Z, Cornish J, Lannigan R
Br J Exp Pathol. 1985 Jun;66(3):357-64.
Rabbits injected with a guinea-pig anti-rabbit kidney fraction 3 antiserum developed immune complex deposition in the glomerulus which disappeared by the sixth day. The distribution of the glomerular deposits was similar to those of passive Heymann nephritis in the rat. A glomerular fixed antigen was not demonstrated in normal rabbit kidneys after perfusion with the guinea-pig anti-tubular antiserum. When tubular antigen was injected intraperitoneally in saline it could be detected in the glomeruli and after injection of the anti-tubular antiserum the deposits stained with increased intensity. Addition of a small amount of anti-GBM antiserum to the anti-tubular antiserum enhanced the size and number of glomerular deposits and increased their survival time. It is concluded that there is no pre-existing tubular antigen in the rabbit glomerulus and that the injected heterologous anti-tubular antiserum releases antigen from an extraglomerular source, probably the proximal tubules, and this released antigen becomes trapped in the glomerulus.
给兔子注射豚鼠抗兔肾3号组分抗血清后,肾小球出现免疫复合物沉积,到第6天时消失。肾小球沉积物的分布与大鼠被动型海曼肾炎相似。用豚鼠抗肾小管抗血清灌注正常兔肾后,未证实肾小球存在固定抗原。当将肾小管抗原溶于生理盐水腹腔注射时,可在肾小球中检测到,注射抗肾小管抗血清后,沉积物染色强度增加。向抗肾小管抗血清中加入少量抗肾小球基底膜抗血清,可增加肾小球沉积物的大小和数量,并延长其存活时间。结论是兔肾小球中不存在预先存在的肾小管抗原,注射的异种抗肾小管抗血清从肾小球外来源(可能是近端小管)释放抗原,释放的抗原被困在肾小球中。