Abstract
Human tumors frequently express membrane-bound or soluble NK group 2, member D (NKG2D) ligands. This results in chronic engagement of NKG2D on the surfaces of NK and CD8(+) T cells and rapid internalization of the receptor. Although it is well appreciated that this phenomenon impairs NKG2D-dependent function, careful analysis of NKG2D-independent functions in cells chronically stimulated through NKG2D is lacking. Using a mouse model of chronic NKG2D ligand expression, we show that constant exposure to NKG2D ligands does not functionally impair NK cells and CD8(+) T cells in the context of viral infection.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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CD8-Positive T-Lymphocytes / immunology
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CD8-Positive T-Lymphocytes / metabolism
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CD8-Positive T-Lymphocytes / virology
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Cell Differentiation / immunology
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Cells, Cultured
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Cytotoxicity Tests, Immunologic
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Killer Cells, Natural / cytology
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Killer Cells, Natural / immunology*
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Killer Cells, Natural / metabolism*
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Killer Cells, Natural / virology
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Ligands
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Lymphocyte Activation / immunology*
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Mice
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Mice, Inbred C57BL
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Mice, Knockout
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Mice, Transgenic
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Muromegalovirus / immunology
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NK Cell Lectin-Like Receptor Subfamily K / antagonists & inhibitors
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NK Cell Lectin-Like Receptor Subfamily K / physiology*
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Nuclear Matrix-Associated Proteins / genetics
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Nuclear Matrix-Associated Proteins / metabolism
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Nuclear Matrix-Associated Proteins / physiology*
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Nucleocytoplasmic Transport Proteins / genetics
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Nucleocytoplasmic Transport Proteins / metabolism
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Nucleocytoplasmic Transport Proteins / physiology*
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Time Factors
Substances
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Klrk1 protein, mouse
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Ligands
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NK Cell Lectin-Like Receptor Subfamily K
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Nuclear Matrix-Associated Proteins
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Nucleocytoplasmic Transport Proteins
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Rae1 protein, mouse