Stimulation of host NKT cells by synthetic glycolipid regulates acute graft-versus-host disease by inducing Th2 polarization of donor T cells

J Immunol. 2005 Jan 1;174(1):551-6. doi: 10.4049/jimmunol.174.1.551.

Abstract

NKT cells are a unique immunoregulatory T cell population that produces large amounts of cytokines. We have investigated whether stimulation of host NKT cells could modulate acute graft-vs-host disease (GVHD) in mice. Injection of the synthetic NKT cell ligand alpha-galactosylceramide (alpha-GalCer) to recipient mice on day 0 following allogeneic bone marrow transplantation promoted Th2 polarization of donor T cells and a dramatic reduction of serum TNF-alpha, a critical mediator of GVHD. A single injection of alpha-GalCer to recipient mice significantly reduced morbidity and mortality of GVHD. However, the same treatment was unable to confer protection against GVHD in NKT cell-deficient CD1d knockout (CD1d(-/-)) or IL-4(-/-) recipient mice or when STAT6(-/-) mice were used as donors, indicating the critical role of host NKT cells, host production of IL-4, and Th2 cytokine responses mediated by donor T cells on the protective effects of alpha-GalCer against GVHD. Thus, stimulation of host NKT cells through administration of NKT ligand can regulate acute GVHD by inducing Th2 polarization of donor T cells via STAT6-dependent mechanisms and might represent a novel strategy for prevention of acute GVHD.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antigens, CD1 / genetics
  • Antigens, CD1d
  • Bone Marrow Transplantation
  • Enzyme-Linked Immunosorbent Assay
  • Female
  • Flow Cytometry
  • Galactosylceramides / immunology*
  • Galactosylceramides / pharmacology
  • Glycolipids / immunology
  • Glycolipids / pharmacology
  • Graft vs Host Disease / immunology
  • Graft vs Host Disease / pathology
  • Graft vs Host Disease / prevention & control*
  • Mice
  • Mice, Knockout
  • STAT6 Transcription Factor
  • T-Lymphocyte Subsets / drug effects
  • T-Lymphocyte Subsets / immunology*
  • T-Lymphocytes / drug effects
  • T-Lymphocytes / immunology*
  • Th2 Cells / immunology*
  • Trans-Activators / deficiency
  • Trans-Activators / genetics
  • Tumor Necrosis Factor-alpha / drug effects
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Antigens, CD1
  • Antigens, CD1d
  • Galactosylceramides
  • Glycolipids
  • STAT6 Transcription Factor
  • Stat6 protein, mouse
  • Trans-Activators
  • Tumor Necrosis Factor-alpha
  • alpha-galactosylceramide