Ligation of OX40 (CD134) regulates graft-versus-host disease (GVHD) and graft rejection in allogeneic bone marrow transplant recipients

Blood. 2003 May 1;101(9):3741-8. doi: 10.1182/blood-2002-10-3048. Epub 2003 Jan 9.

Abstract

OX40 (CD134) is expressed on activated T cells; its ligand, OX40 ligand (OX40L) is expressed on dendritic cells, B cells, and activated endothelial cells. To determine how OX40-OX40L interaction affects graft-versus-host disease (GVHD), we used antagonistic anti-OX40L monoclonal antibody (mAb) or OX40(-/-) donor or OX40L(-/-) recipient mice. Similar degrees of GVHD reduction were observed with each approach. Despite the fact that OX40 is up-regulated on both CD4(+) and CD8(+) T cells isolated during GVHD, the major effects of OX40 ligation were on CD4(+) and not CD8(+) T-cell-mediated alloresponses as assessed in both GVHD and engraftment model systems. GVHD inhibition by blockade of the OX40/OX40L pathway did not require CD28 signaling. Some studies have indicated OX40 is essential for inducing T-helper type 2 (Th2) responses. However, in vivo blockade of OX40-OX40L interactions reduced GVHD mortality induced by either signal transducer and activator of transcription-6(-/-) (Stat-6(-/-)) (Th2-defective) or Stat-4(-/-) (Th1-defective) major histocompatibility complex (MHC)-disparate splenocytes, indicating that the GVHD-ameliorating effects did not require Stat-4 or Stat-6 signaling. Although OX40L has been reported to be expressed on activated T cells, no effects on GVHD were observed when OX40L(-/-) versus OX40L(+/+) T cells were infused in different models. These data provide insights as to the mechanisms responsible for OX40/OX40L regulation of GVHD.

Publication types

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

MeSH terms

  • Animals
  • Antibodies, Monoclonal / immunology
  • Antibodies, Monoclonal / pharmacology
  • Antibody Specificity
  • Bone Marrow Transplantation*
  • CD28 Antigens / physiology
  • CD4-Positive T-Lymphocytes / immunology*
  • CD4-Positive T-Lymphocytes / transplantation
  • CD8-Positive T-Lymphocytes / immunology
  • CD8-Positive T-Lymphocytes / transplantation
  • Crosses, Genetic
  • DNA-Binding Proteins / deficiency
  • DNA-Binding Proteins / genetics
  • DNA-Binding Proteins / physiology
  • Dendritic Cells / immunology
  • Graft Rejection / immunology*
  • Graft vs Host Disease / immunology*
  • Graft vs Host Disease / prevention & control
  • Membrane Glycoproteins / immunology*
  • Mice
  • Mice, Inbred BALB C
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Mice, SCID
  • OX40 Ligand
  • Radiation Chimera
  • Receptors, OX40
  • Receptors, Tumor Necrosis Factor*
  • STAT4 Transcription Factor
  • STAT6 Transcription Factor
  • Signal Transduction
  • Specific Pathogen-Free Organisms
  • Th1 Cells / immunology
  • Th2 Cells / immunology
  • Trans-Activators / deficiency
  • Trans-Activators / genetics
  • Trans-Activators / physiology
  • Transplantation, Homologous / immunology*
  • Tumor Necrosis Factor Receptor Superfamily, Member 7 / immunology*
  • Tumor Necrosis Factors

Substances

  • Antibodies, Monoclonal
  • CD28 Antigens
  • DNA-Binding Proteins
  • Membrane Glycoproteins
  • OX40 Ligand
  • Receptors, OX40
  • Receptors, Tumor Necrosis Factor
  • STAT4 Transcription Factor
  • STAT6 Transcription Factor
  • Stat4 protein, mouse
  • Stat6 protein, mouse
  • Tnfrsf4 protein, mouse
  • Tnfsf4 protein, mouse
  • Trans-Activators
  • Tumor Necrosis Factor Receptor Superfamily, Member 7
  • Tumor Necrosis Factors