Antibody-induced transplant arteriosclerosis is prevented by graft expression of anti-oxidant and anti-apoptotic genes View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1998-12

AUTHORS

W W Hancock, R Buelow, M H Sayegh, L A Turka

ABSTRACT

We investigated the pathogenesis of chronic allograft rejection in mouse cardiac allografts. Long-term survival occurred after administration of monoclonal antibody to CD4 or CD40-ligand (CD40L) plus donor cells. Both treatments induced permanent graft survival, but, in contrast to transplants in mice treated with CD4 monoclonal antibody, grafts in mice treated with CD40L monoclonal antibody lacked evidence of chronic rejection, including transplant arteriosclerosis. Freedom from chronic rejection in the group treated with CD40L monoclonal antibody correlated with vascular expression of the 'protective' genes heme oxygenase-1 (HO-1), Bcl-xL and A20. Moreover, arteriosclerosis was induced in allografts in immunoglobulin-deficient mice by antibody transfer only when the transfer was done before expression of protective genes. A direct role for protective gene expression in endothelial cells was demonstrated by in vitro experiments in which induction of HO-1 or Bcl-xL suppressed alloantibody-stimulated endothelial activation. Finally, induction of HO-1 in vivo protected allografts against chronic injury. These data show a role for protective genes in the prevention of chronic rejection, and indicate new approaches to protect grafts against development of transplant arteriosclerosis. More... »

PAGES

1392-1396

Journal

TITLE

Nature Medicine

ISSUE

12

VOLUME

4

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/3982

DOI

http://dx.doi.org/10.1038/3982

DIMENSIONS

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PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/9846576


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