Abstract
Natural killer T (NKT) cells express a T cell receptor (TCR) and markers common to NK cells, including NK1.1. In vivo, NKT cells are triggered by anti-CD3epsilon MAb to rapidly produce large amounts of IL-4 and by IL-12 to reject tumors. We show here that anti-CD3epsilon MAb treatment rapidly depletes the liver (and partially the spleen) of NKT cells and that homeostasis is achieved 1 to 2 days later via NKT cell proliferation that occurs mainly in bone marrow. Similar results were obtained in mice treated with IL-12. Collectively, our data demonstrate that peripheral NKT cells are highly sensitive to activation-induced cell death and that bone marrow plays a major role in restoring NKT cell homeostasis.
MeSH terms
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Animals
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Antibodies, Monoclonal / administration & dosage
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Antibodies, Monoclonal / analysis
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Antibodies, Monoclonal / pharmacology*
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Antigens / analysis
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Antigens, Ly
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Antigens, Surface
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Apoptosis
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Bone Marrow / physiology
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CD3 Complex / immunology*
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Cell Death / drug effects
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Cell Division / drug effects
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Female
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Homeostasis
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Interleukin-12 / administration & dosage
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Interleukin-12 / pharmacology*
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Killer Cells, Natural / cytology*
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Lectins, C-Type
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Liver / cytology
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Lymphocyte Activation
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Mice
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Mice, Inbred C57BL
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NK Cell Lectin-Like Receptor Subfamily B
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Proteins / analysis
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Spleen / cytology
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T-Lymphocytes / cytology*
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T-Lymphocytes / drug effects*
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T-Lymphocytes / physiology
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Thymus Gland / cytology
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Thymus Gland / physiology
Substances
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Antibodies, Monoclonal
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Antigens
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Antigens, Ly
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Antigens, Surface
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CD3 Complex
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Klrb1c protein, mouse
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Lectins, C-Type
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NK Cell Lectin-Like Receptor Subfamily B
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Proteins
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Interleukin-12