CD8 T cell-mediated rejection of intestinal allografts is resistant to inhibition of the CD40/CD154 costimulatory pathway

Transplantation. 2001 May 15;71(9):1351-4. doi: 10.1097/00007890-200105150-00033.

Abstract

Background: Disruption of the CD40/CD154 pathway inhibits rejection in numerous models. The importance of this pathway on intestinal allograft rejection was examined in this study.

Methods: Intestinal grafts from B6C3F1 mice transplanted into C57BL/6 recipients were assessed histologically for rejection.

Results: The monoclonal antibody to CD154, MR1, failed to inhibit rejection in wild-type mice. Similarly, CD154-/- recipient mice rejected intestinal allografts. MR1 did inhibit early rejection in CD8-/- mice, but had no effect in CD4-/- recipients. All MR1-treated CD8-/- recipients eventually developed rejection. No benefit was observed when blockade of the CD40/CD154 pathway by MR1 was combined with blockade of the CD28/B7 pathway by mCTLA4Ig.

Conclusions: These data suggest that CD4+ T cells mediating intestinal allograft rejection may be more dependent upon the CD40/CD154 pathway than CD8+ T cells. This finding highlights the importance of identifying agents that suppress CD8+ T cell-mediated rejection.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Antibodies, Monoclonal / therapeutic use
  • CD4-Positive T-Lymphocytes / physiology
  • CD40 Antigens / immunology
  • CD40 Antigens / physiology*
  • CD40 Ligand / immunology
  • CD40 Ligand / physiology*
  • CD8-Positive T-Lymphocytes / physiology
  • Graft Rejection / prevention & control
  • Graft Survival / physiology
  • Intestine, Small / transplantation*
  • Jejunum / transplantation
  • Mice
  • Mice, Inbred C57BL
  • RNA, Messenger / metabolism
  • Signal Transduction / drug effects
  • Signal Transduction / physiology
  • Transplantation, Homologous / immunology
  • Transplantation, Homologous / pathology

Substances

  • Antibodies, Monoclonal
  • CD40 Antigens
  • RNA, Messenger
  • CD40 Ligand