help button home button Am J Pathol sign up for etoc
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Order Full text via Infotrieve
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Quigg, R. J.
Right arrow Articles by Salant, D. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Quigg, R. J.
Right arrow Articles by Salant, D. J.

American Journal of Pathology, Vol 134, 1125-1133, Copyright © 1989 by American Society for Investigative Pathology


REGULAR ARTICLES

Studies with antibodies to cultured rat glomerular epithelial cells. Subepithelial immune deposit formation after in vivo injection

RJ Quigg, DR Abrahamson, AV Cybulsky, J Badalamenti, AW Minto and DJ Salant
Evans Memorial Department of Clinical Research, University Hospital, Boston University Medical Center, Massachusetts.

To investigate the role of glomerular epithelial cell (GEC) membrane proteins in the in situ formation of subepithelial immune deposits, the authors raised a rabbit antiserum against GEC that had been grown in culture (anti-GEC). By indirect immunofluorescence (IF) on normal rat kidney, anti-GEC stained proximal tubular brush border (BB). After intravenous injection into animals, granular glomerular capillary wall staining for IgG was present by IE and subepithelial immune deposits were identified by standard transmission and immunoelectron microscopy. Using the latter technique, injected anti-GEC IgG was identified beneath slit diaphragms and in endocytic-coated pits and intracellular vesicles of podocytes. Anti-GEC immunoprecipitated gp330 and two other proteins from radiolabeled BB. These proteins also were identified by sheep anti-rat Fx1A, the antiserum responsible for passive Heymann nephritis. Anti-GEC and anti-Fx1A also immunoprecipitated five identical proteins from surface-labeled GEC. Biosynthetically-labeled but not surface-labeled GEC contained immunoprecipitable gp330. Thus, injection into rats of antibodies raised against cultured GEC can produce subepithelial immune deposits, a disease process classically induced by antibodies to BB or its purified components. In addition to gp330, GEC and BB share other antigenic determinants that may contribute to the formation of these immune deposits.


This article has been cited by other articles:


Home page
J. Immunol.Home page
L. Bao, M. Haas, S. A. Boackle, D. M. Kraus, P. N. Cunningham, P. Park, J. J. Alexander, R. K. Anderson, K. Culhane, V. M. Holers, et al.
Transgenic Expression of a Soluble Complement Inhibitor Protects Against Renal Disease and Promotes Survival in MRL/lpr Mice
J. Immunol., April 1, 2002; 168(7): 3601 - 3607.
[Abstract] [Full Text] [PDF]


Home page
J. Am. Soc. Nephrol.Home page
P. PARK, M. HAAS, P. N. CUNNINGHAM, J. J. ALEXANDER, L. BAO, J. M. GUTHRIDGE, D. M. KRAUS, V. M. HOLERS, and R. J. QUIGG
Inhibiting the Complement System Does Not Reduce Injury in Renal Ischemia Reperfusion
J. Am. Soc. Nephrol., July 1, 2001; 12(7): 1383 - 1390.
[Abstract] [Full Text] [PDF]


Home page
J. Am. Soc. Nephrol.Home page
B. SCHILLER, P. N. CUNNINGHAM, J. J. ALEXANDER, L. BAO, V. M. HOLERS, and R. J. QUIGG
Expression of a Soluble Complement Inhibitor Protects Transgenic Mice from Antibody-Induced Acute Renal Failure
J. Am. Soc. Nephrol., January 1, 2001; 12(1): 71 - 79.
[Abstract] [Full Text]


Home page
JEMHome page
R. J. Quigg, C. He, A. Lim, D. Berthiaume, J. J. Alexander, D. Kraus, and V. Michael Holers
Transgenic Mice Overexpressing the Complement Inhibitor Crry as a Soluble Protein Are Protected from Antibody-induced Glomerular Injury
J. Exp. Med., October 5, 1998; 188(7): 1321 - 1331.
[Abstract] [Full Text] [PDF]


Home page
JEMHome page
B. Schiller, C. He, D. J. Salant, A. Lim, J. J. Alexander, and R. J. Quigg
Inhibition of Complement Regulation Is Key to the Pathogenesis of Active Heymann Nephritis
J. Exp. Med., October 5, 1998; 188(7): 1353 - 1358.
[Abstract] [Full Text] [PDF]


Home page
J. Immunol.Home page
R. J. Quigg, Y. Kozono, D. Berthiaume, A. Lim, D. J. Salant, A. Weinfeld, P. Griffin, E. Kremmer, and V. M. Holers
Blockade of Antibody-Induced Glomerulonephritis with Crry-Ig, a Soluble Murine Complement Inhibitor
J. Immunol., May 1, 1998; 160(9): 4553 - 4560.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Renal Physiol.Home page
P. Park, M. Haas, P. N. Cunningham, L. Bao, J. J. Alexander, and R. J. Quigg
Injury in renal ischemia-reperfusion is independent from immunoglobulins and T lymphocytes
Am J Physiol Renal Physiol, February 1, 2002; 282(2): F352 - F357.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1989 by the American Society for Investigative Pathology.