Abstract
Acute graft-versus-host disease (aGVHD) remains a major complication of allogeneic bone marrow transplantation, which is caused by donor T cells specific for host alloantigens. In a murine model, we found that donor T cells expressed a natural killer cell inhibitory receptor, CD94/NKG2A, during the course of aGVHD. Administration of an anti-NKG2A mAb markedly inhibited the expansion of donor T cells and ameliorated the aGVHD pathologies. These results suggested that the CD94/NKG2A inhibitory receptor expressed on host-reactive donor T cells can be a novel target for the amelioration of aGVHD.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Acute Disease
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Animals
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Antibodies, Monoclonal / therapeutic use
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Antigens, CD / biosynthesis
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Antigens, CD / genetics
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Antigens, CD / immunology
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Cell Proliferation / drug effects
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Cytotoxicity, Immunologic / immunology
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Female
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Graft vs Host Disease / immunology*
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Graft vs Host Disease / pathology
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Graft vs Host Disease / therapy*
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Lectins, C-Type / biosynthesis
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Lectins, C-Type / genetics
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Lectins, C-Type / immunology
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Mice
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Mice, Inbred BALB C
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Mice, Inbred C57BL
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NK Cell Lectin-Like Receptor Subfamily C
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NK Cell Lectin-Like Receptor Subfamily D
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Receptors, Immunologic / biosynthesis
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Receptors, Immunologic / immunology*
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Receptors, Immunologic / metabolism
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Receptors, Natural Killer Cell
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T-Lymphocytes / immunology*
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T-Lymphocytes / metabolism
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T-Lymphocytes / transplantation
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T-Lymphocytes, Cytotoxic / immunology
Substances
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Antibodies, Monoclonal
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Antigens, CD
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Klrc1 protein, mouse
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Klrd1 protein, mouse
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Lectins, C-Type
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NK Cell Lectin-Like Receptor Subfamily C
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NK Cell Lectin-Like Receptor Subfamily D
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Receptors, Immunologic
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Receptors, Natural Killer Cell