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Prevention of Experimental Autoimmune Encephalomyelitis by Transfer of Embryonic Stem Cell-Derived Dendritic Cells Expressing Myelin Oligodendrocyte Glycoprotein Peptide along with TRAIL or Programmed Death-1 Ligand

Shinya Hirata, Satoru Senju, Hidetake Matsuyoshi, Daiki Fukuma, Yasushi Uemura and Yasuharu Nishimura
J Immunol February 15, 2005, 174 (4) 1888-1897; DOI: https://doi.org/10.4049/jimmunol.174.4.1888
Shinya Hirata
Department of Immunogenetics, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan
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Satoru Senju
Department of Immunogenetics, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan
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Hidetake Matsuyoshi
Department of Immunogenetics, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan
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Daiki Fukuma
Department of Immunogenetics, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan
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Yasushi Uemura
Department of Immunogenetics, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan
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Yasuharu Nishimura
Department of Immunogenetics, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan
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Abstract

Experimental autoimmune encephalomyelitis (EAE) is caused by activation of myelin Ag-reactive CD4+ T cells. In the current study, we tested a strategy to prevent EAE by pretreatment of mice with genetically modified dendritic cells (DC) presenting myelin oligodendrocyte glycoprotein (MOG) peptide in the context of MHC class II molecules and simultaneously expressing TRAIL or Programmed Death-1 ligand (PD-L1). For genetic modification of DC, we used a recently established method to generate DC from mouse embryonic stem cells (ES cells) in vitro (ES-DC). ES cells were sequentially transfected with an expression vector for TRAIL or PD-L1 and an MHC class II-associated invariant chain-based MOG epitope-presenting vector. Subsequently, double-transfectant ES cell clones were induced to differentiate to ES-DC, which expressed the products of introduced genes. Treatment of mice with either of the double-transfectant ES-DC significantly reduced T cell response to MOG, cell infiltration into spinal cord, and the severity of MOG peptide-induced EAE. In contrast, treatment with ES-DC expressing MOG alone, irrelevant Ag (OVA) plus TRAIL, or OVA plus PD-L1, or coinjection with ES-DC expressing MOG plus ES-DC-expressing TRAIL or PD-L1 had no effect in reducing the disease severity. In contrast, immune response to irrelevant exogenous Ag (keyhole limpet hemocyanin) was not impaired by treatment with any of the genetically modified ES-DC. The double-transfectant ES-DC presenting Ag and simultaneously expressing immune-suppressive molecules may well prove to be an effective therapy for autoimmune diseases without inhibition of the immune response to irrelevant Ag.

  • Received May 20, 2004.
  • Accepted December 8, 2004.
  • Copyright © 2005 by The American Association of Immunologists
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The Journal of Immunology: 174 (4)
The Journal of Immunology
Vol. 174, Issue 4
15 Feb 2005
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Prevention of Experimental Autoimmune Encephalomyelitis by Transfer of Embryonic Stem Cell-Derived Dendritic Cells Expressing Myelin Oligodendrocyte Glycoprotein Peptide along with TRAIL or Programmed Death-1 Ligand
Shinya Hirata, Satoru Senju, Hidetake Matsuyoshi, Daiki Fukuma, Yasushi Uemura, Yasuharu Nishimura
The Journal of Immunology February 15, 2005, 174 (4) 1888-1897; DOI: 10.4049/jimmunol.174.4.1888

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Prevention of Experimental Autoimmune Encephalomyelitis by Transfer of Embryonic Stem Cell-Derived Dendritic Cells Expressing Myelin Oligodendrocyte Glycoprotein Peptide along with TRAIL or Programmed Death-1 Ligand
Shinya Hirata, Satoru Senju, Hidetake Matsuyoshi, Daiki Fukuma, Yasushi Uemura, Yasuharu Nishimura
The Journal of Immunology February 15, 2005, 174 (4) 1888-1897; DOI: 10.4049/jimmunol.174.4.1888
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