Natorio Y, Hayakawa I, Shibata S
Division of Pathophysiology, National Medical Center, Tokyo, Japan.
Am J Pathol. 1989 Feb;134(2):405-10.
Injection of antibodies to renal tubular membrane (Fx1A) into Lewis rats induces granular deposits of IgG in glomeruli and proteinuria (passive Heymann nephritis, PHN), and similar lesions are also induced by antibody to one of the antigens in Fx1A, dipeptidyl peptidase IV (DPP IV, gp 108). In this study, the role of DPP IV in PHN was investigated using DPP IV-deficient F344 rats. The amount of DPP IV found in F344 rat kidneys was less than 0.05% of that present in Wistar rats, and injection of anti-DPP IV antibody into F344 rats did not induce proteinuria. Injection of anti-F344 Fx1A rabbit antibodies that contain no detectable anti-DPP IV antibody into Lewis or F344 rats induced PHN, characterized by granular deposits of rabbit IgG in glomeruli and massive proteinuria, although the appearance of proteinuria was delayed in comparison with that occurring in response to injection of anti-Wistar Fx1A antibodies. These results indicate that DPP IV may contribute to, but is not essential for, the induction of PHN.
将抗肾小管膜抗体(Fx1A)注射到Lewis大鼠体内会诱导肾小球中IgG颗粒沉积和蛋白尿(被动型Heymann肾炎,PHN),并且抗Fx1A中的一种抗原二肽基肽酶IV(DPP IV,糖蛋白108)的抗体也会诱导类似病变。在本研究中,使用DPP IV缺陷型F344大鼠研究了DPP IV在PHN中的作用。F344大鼠肾脏中发现的DPP IV量不到Wistar大鼠的0.05%,并且将抗DPP IV抗体注射到F344大鼠体内不会诱导蛋白尿。将不含可检测到的抗DPP IV抗体的抗F344 Fx1A兔抗体注射到Lewis或F344大鼠体内会诱导PHN,其特征是肾小球中有兔IgG颗粒沉积和大量蛋白尿,尽管与注射抗Wistar Fx1A抗体相比,蛋白尿出现的时间延迟。这些结果表明DPP IV可能有助于PHN的诱导,但不是必需的。