Suppression of xenogeneic graft-versus-host disease by treatment with immunoglobulin-like transcript 3-Fc

Hum Immunol. 2009 Sep;70(9):663-9. doi: 10.1016/j.humimm.2009.06.001. Epub 2009 Jun 6.

Abstract

Allogeneic hematopoietic cell transplantation represents an important therapy for certain malignant and nonmalignant diseases. However, graft-versus-host disease (GVHD) is a major cause of mortality and morbidity. The search for agents that can efficiently suppress GVHD has been going on for more than half a century. GVHD is particularly strong in xenogeneic donor-recipient combinations, given the unlimited number of potentially immunogenic antigens donor lymphocytes encounter in the host. Using a hu-nonobese diabetic/severe combined immunodeficiency (hu-NOD/SCID) gamma-null model of xenogeneic GVHD, we have demonstrated that treatment with recombinant immunoglobulin-like transcript 3-Fc protein induces the differentiation of CD8(+) T suppressor cells and blocks the cellular and humoral arm of the GVH reaction.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antibodies, Heterophile / immunology
  • Antigens, Heterophile / immunology
  • CD8-Positive T-Lymphocytes / immunology
  • CD8-Positive T-Lymphocytes / metabolism
  • CD8-Positive T-Lymphocytes / pathology
  • Cell Differentiation / genetics
  • Disease Progression
  • Female
  • Genetic Engineering
  • Graft vs Host Disease / immunology*
  • Graft vs Host Disease / physiopathology
  • Graft vs Host Disease / therapy
  • Hematopoietic Stem Cell Transplantation
  • Humans
  • Immunoglobulin Fc Fragments / genetics
  • Immunoglobulin Fc Fragments / immunology
  • Immunoglobulin Fc Fragments / metabolism*
  • Immunosuppressive Agents / immunology
  • Immunosuppressive Agents / metabolism
  • Immunotherapy*
  • Membrane Glycoproteins
  • Mice
  • Mice, Inbred NOD
  • Mice, SCID
  • Radiation Chimera
  • Receptors, Cell Surface / genetics
  • Receptors, Cell Surface / immunology
  • Receptors, Cell Surface / metabolism*
  • Receptors, Immunologic
  • Recombinant Fusion Proteins / genetics
  • Recombinant Fusion Proteins / immunology
  • Recombinant Fusion Proteins / metabolism*
  • T-Lymphocytes, Regulatory / immunology
  • T-Lymphocytes, Regulatory / metabolism
  • T-Lymphocytes, Regulatory / pathology

Substances

  • Antibodies, Heterophile
  • Antigens, Heterophile
  • Immunoglobulin Fc Fragments
  • Immunosuppressive Agents
  • LILRB4 protein, human
  • Membrane Glycoproteins
  • Receptors, Cell Surface
  • Receptors, Immunologic
  • Recombinant Fusion Proteins