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

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.
AuthorsGeorge Vlad, Michael B Stokes, Zhuoru Liu, Chih-Chao Chang, Hugo Sondermeijer, Elena R Vasilescu, Adriana I Colovai, Pasquale Berloco, Vivette D D'Agati, Lloyd Ratner, Raffaello Cortesini, Nicole Suciu-Foca
JournalHuman immunology (Hum Immunol) Vol. 70 Issue 9 Pg. 663-9 (Sep 2009) ISSN: 1879-1166 [Electronic] United States
PMID19501624 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Antibodies, Heterophile
  • Antigens, Heterophile
  • Immunoglobulin Fc Fragments
  • Immunosuppressive Agents
  • LILRB4 protein, human
  • Membrane Glycoproteins
  • Receptors, Cell Surface
  • Receptors, Immunologic
  • Recombinant Fusion Proteins
Topics
  • Animals
  • Antibodies, Heterophile (immunology)
  • Antigens, Heterophile (immunology)
  • CD8-Positive T-Lymphocytes (immunology, metabolism, pathology)
  • Cell Differentiation (genetics)
  • Disease Progression
  • Female
  • Genetic Engineering
  • Graft vs Host Disease (immunology, physiopathology, therapy)
  • Hematopoietic Stem Cell Transplantation
  • Humans
  • Immunoglobulin Fc Fragments (genetics, immunology, metabolism)
  • Immunosuppressive Agents (immunology, metabolism)
  • Immunotherapy
  • Membrane Glycoproteins
  • Mice
  • Mice, Inbred NOD
  • Mice, SCID
  • Radiation Chimera
  • Receptors, Cell Surface (genetics, immunology, metabolism)
  • Receptors, Immunologic
  • Recombinant Fusion Proteins (genetics, immunology, metabolism)
  • T-Lymphocytes, Regulatory (immunology, metabolism, pathology)

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