Loss of B7-H1 expression by recipient parenchymal cells leads to expansion of infiltrating donor CD8+ T cells and persistence of graft-versus-host disease

J Immunol. 2012 Jan 15;188(2):724-34. doi: 10.4049/jimmunol.1102630. Epub 2011 Dec 12.

Abstract

Previous experimental studies have shown that acute graft-versus-host disease (GVHD) is associated with two waves of donor CD8(+) T cell expansion. In the current studies, we used in vivo bioluminescent imaging, in vivo BrdU labeling, and three different experimental GVHD systems to show that B7-H1 expression by recipient parenchymal cells controls the second wave of alloreactive donor CD8(+) T cell expansion and the associated second phase of GVHD. Loss of B7-H1 expression by parenchymal cells during the course of GVHD was associated with persistent proliferation of donor CD8(+) T cells in GVHD target tissues and continued tissue injury, whereas persistent expression of B7-H1 expression by parenchymal cells led to reduced proliferation of donor CD8(+) T cells in GVHD target tissues and resolution of GVHD. These studies demonstrate that parenchymal cell expression of B7-H1 is required for tolerizing infiltrating T cells and preventing the persistence of GVHD. Our results suggest that therapies designed to preserve or restore expression of B7-H1 expression by parenchymal tissues in the recipient could prevent or ameliorate GVHD in humans.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • B7-H1 Antigen / deficiency*
  • B7-H1 Antigen / genetics*
  • B7-H1 Antigen / physiology
  • CD8-Positive T-Lymphocytes / immunology*
  • CD8-Positive T-Lymphocytes / pathology
  • CD8-Positive T-Lymphocytes / transplantation*
  • Cell Movement / genetics
  • Cell Movement / immunology*
  • Cell Proliferation*
  • Graft Survival / genetics
  • Graft Survival / immunology
  • Graft vs Host Disease / immunology*
  • Graft vs Host Disease / pathology
  • Hepatocytes / immunology*
  • Hepatocytes / metabolism
  • Hepatocytes / pathology
  • Liver Transplantation / immunology
  • Liver Transplantation / methods
  • Liver Transplantation / pathology
  • Lymphocyte Activation / genetics
  • Lymphocyte Activation / immunology
  • Mice
  • Mice, Inbred BALB C
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Mice, Transgenic
  • Transplantation Tolerance / genetics
  • Transplantation Tolerance / immunology
  • Up-Regulation / genetics
  • Up-Regulation / immunology

Substances

  • B7-H1 Antigen
  • Cd274 protein, mouse