Abstract
The natural killer (NK) cell activation receptor Ly49H is required for resistance to murine cytomegalovirus (MCMV). We show here that NK cell proliferation and production of interferon-gamma (IFN-gamma) was not dependent on Ly49H expression during early MCMV infection. During a later phase of infection, however, Ly49H+ NK cells selectively proliferated and this expansion was blocked by anti-Ly49H administration. With vaccinia virus infection, neither the early nor late phase of NK cell proliferation was selective for Ly49H+ NK cells. These findings indicated that Ly49H+ NK cells were specifically activated by MCMV and that MCMV infection was characterized by nonspecific and specific phases of NK cell activation in vivo.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Antibodies, Monoclonal / pharmacology
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Antigens, Ly*
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Cells, Cultured
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Herpesviridae Infections / immunology*
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Interferon-gamma / biosynthesis
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Killer Cells, Natural / immunology*
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Kinetics
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Lectins, C-Type
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Lymphocyte Activation*
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Lymphocyte Subsets / classification
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Lymphocyte Subsets / immunology
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Membrane Glycoproteins / immunology
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Membrane Glycoproteins / metabolism
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Mice
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Mice, Inbred C57BL
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NK Cell Lectin-Like Receptor Subfamily A
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Receptors, NK Cell Lectin-Like
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Vaccinia / immunology
Substances
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Antibodies, Monoclonal
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Antigens, Ly
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Klra8 protein, mouse
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Lectins, C-Type
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Membrane Glycoproteins
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NK Cell Lectin-Like Receptor Subfamily A
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Receptors, NK Cell Lectin-Like
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Interferon-gamma