Natori Y, Shindo N, Natori Y
Division of Pathophysiology, National Medical Centre, Tokyo, Japan.
Clin Exp Immunol. 1994 Feb;95(2):327-32. doi: 10.1111/j.1365-2249.1994.tb06532.x.
Massive proteinuria is induced in rats by administration of rabbit antibody to dipeptidyl peptidase IV (DPPIV, gp108), a glycoprotein present on glomerular cell membranes and in serum. This study was undertaken to know which antigen, glomerular or serum DPPIV, is responsible for forming immune complex in glomeruli and development of proteinuria. An i.p. injection of the antibody resulted in a rapid decrease of serum DPPIV and a gradual increase of rabbit IgG deposited along glomerular capillary wall for 4-8 h. Abnormal proteinuria appeared within 8 h, peaked on day 2 (> 200 mg/24 h) and then declined. An increase of urinary protein and glomerular deposition of IgG also occurred, when the antibody was injected into serum DPPIV-depleted rats that had received preinjection of anti-DPPIV antibody. These results suggest that proteinuria is induced by direct binding of anti-DPPIV antibody to the membrane antigen of glomerular cells.
通过给大鼠注射抗二肽基肽酶IV(DPPIV,gp108)的兔抗体可诱导大鼠出现大量蛋白尿,DPPIV是一种存在于肾小球细胞膜和血清中的糖蛋白。本研究旨在明确是哪种抗原,即肾小球DPPIV还是血清DPPIV,负责在肾小球中形成免疫复合物以及蛋白尿的发展。腹腔注射该抗体导致血清DPPIV迅速减少,兔IgG沿肾小球毛细血管壁的沉积在4 - 8小时内逐渐增加。异常蛋白尿在8小时内出现,在第2天达到峰值(> 200 mg/24小时),然后下降。当将抗体注射到预先注射了抗DPPIV抗体的血清DPPIV缺失的大鼠中时,也会出现尿蛋白增加和IgG在肾小球的沉积。这些结果表明,蛋白尿是由抗DPPIV抗体与肾小球细胞膜抗原的直接结合所诱导的。