Organ Transplantation Research Today is a free monthly online journal that collates and summarizes the latest research about Organ Transplantation, including details on risks, prognosis, procedure, surgery.

Glutathione depletion of stimulator cells inhibits responder T-cell immunogenicity in vitro and prolongs allograft survival in vivo.

McKenna GJ, Kim PT, Mui AL, Ong CJ, Rotstein OD, Warnock GL, Chung SW

Department of Surgery, University of British Columbia, 3100-910 West 10th Avenue, Vancouver, BC, Canada, V5Z 4E3.

BACKGROUND: Pretransplant donor-organ immunomodulation may attenuate allograft rejection by changing the redox state of donor cells. This study explored impact of donor-cell redox-state alteration by glutathione (GSH) depletion on graft immunogenicity. METHODS: Splenic and heart endothelial cells from Balb/c mice were treated with diethylmaleate (a GSH-depleting agent) and/or lipopolysaccharide to assess the impact of GSH depletion on alloreactivity by mixed lymphocyte reaction, endothelial cell adhesion by T-cell adhesion assay, intracellular adhesion molecule-1 expression by reverse transcriptionase-polymerase chain reaction, and nuclear factor-kappa B upregulation by electrophoretic mobility shift assay. Heterotopic heart transplants were performed as in vivo correlate. RESULTS: GSH depletion decreased endothelial cell and splenic cell alloreactivity, decreased endothelial cell intracellular adhesion molecule-1 expression through attenuation of nuclear factor-kappa B activity, decreased endothelial cell adhesion, and prolonged heterotopic heart transplant graft survival. CONCLUSIONS: GSH depletion may represent a significant immunomodulator of donor antigenicity to prevent transplant rejection.

Published 1 May 2006 in Am J Surg, 191(5): 588-92.
Full-text of this article is available online (may require subscription).

© 2004-2008 Organ Transplantation Research Today. All Rights Reserved.