The Journal of Experimental Medicine
Torrey Pines Biolabs
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents
This Article
Right arrow Alert me when this article is cited
Services
Right arrow Email this article
Right arrow Similar articles in this journal
Right arrow Alert me to new content in the JEM
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Milgrom, F.
Right arrow Articles by Fuji, H.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Milgrom, F.
Right arrow Articles by Fuji, H.
Social Bookmarking
Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?
The Journal of Experimental Medicine, Vol 134, 193-207, Copyright © 1971 by The Rockefeller University Press

IMMUNE COMPLEXES AND GLOMERULONEPHRITIS IN MAN

IMMUNOLOGIC INJURY OF RENAL HOMOGRAFTS

F. Milgrom 1, J. Klassen 1, and H. Fuji 1

1 From the Department of Microbiology, School of Medicine, State University of New York at Buffalo, Buffalo, New York 14214

Rejection of renal allografts in man and animals is most frequently induced by cell-mediated immunity, the morphologic hallmark of which is the infiltration of the graft by mononuclear cells. In some presensitized recipients rejection may be mediated by humoral transplantation antibodies, and this is characterized clinically by a rapid tempo of rejection and morphologically by accumulation of polymorphonuclear neutrophils and renal cortical necrosis.

In recipients treated with immunosuppressive drugs, most renal allografts function well for over 1 yr. However, late deterioration is observed in many grafts. This may take the form of proliferative glomerulonephritis with accumulation of immunoglobulin and complement along glomerular basement membranes. This glomerular lesion of the graft may be of immunologic nature without being rejection. In many instances the glomerular lesion may be due to recurrence of the original disease of the recipient. In other instances it may represent a de novo immunologic process induced by the response to antigens shared by the graft and recipient as evidenced by animal experiments.

The glomerular lesion in the graft may also be caused by humoral transplantation antibodies. Therefore, the final outcome of the renal transplantation may to a great extent depend on the strength of transplantation antibody response, being more favorable for low than high responders.


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?




  Home | Help | Feedback | Subscriptions | Archive | Search
TABLE OF CONTENTS