| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
American Journal of Pathology, Vol 134, 405-410, Copyright © 1989 by American Society for Investigative Pathology
REGULAR ARTICLES |
Y Natorio, I Hayakawa and S Shibata
Division of Pathophysiology, National Medical Center, Tokyo, Japan.
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.
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |