Fas mediates cardiac allograft acceptance in mice with impaired T-cell-intrinsic NF-kappaB signaling

Transpl Int. 2009 Aug;22(8):845-52. doi: 10.1111/j.1432-2277.2009.00875.x. Epub 2009 Apr 1.

Abstract

The transcription factor NF-kappaB is critical for T-cell activation and survival. We have shown that mice expressing a T-cell-restricted NF-kappaB superrepressor (IkappaBalphaDeltaN-Tg) permanently accept heart but not skin allografts. Overexpression of the prosurvival factor Bcl-x(L) in T cells restored heart rejection, suggesting that graft acceptance in IkappaBalphaDeltaN-Tg mice was attributable to deletion of alloreactive T cells.In vitro, the increased death of IkappaBalphaDeltaN-Tg T cells upon TCR stimulation when compared with wildtype T cells was mostly because of Fas/FasL interaction. Similarly, Fas played a key role in cardiac allograft acceptance by IkappaBalphaDeltaN-Tg mice as both genetic and antibody-mediated inhibition of Fas-signaling restored cardiac allograft rejection. Rejection correlated with graft infiltration by T cells and splenic production of IFN-gamma upon allostimulation. These results indicate that T-cell inhibition of NF-kappaB results in cardiac allograft acceptance because of increased susceptibility to Fas-mediated cell death.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Apoptosis
  • Fas Ligand Protein / immunology
  • Graft Rejection / immunology
  • Heart Transplantation / immunology*
  • I-kappa B Proteins / physiology
  • Mice
  • Mice, Inbred BALB C
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • NF-kappa B / physiology*
  • Signal Transduction
  • T-Lymphocytes / immunology*
  • Transplantation, Homologous / physiology
  • fas Receptor / physiology*

Substances

  • Fas Ligand Protein
  • I-kappa B Proteins
  • NF-kappa B
  • fas Receptor