Abstract
The expression and function of cannabinoid receptor 1 (CB1) in mouse immune cells is unclear. Here we show that splenic B cells express more CB1 mRNA than T cells. Furthermore, splenocytes stimulated with the T cell mitogens, PMA/Io and anti-CD3, showed a decrease in CB1 message while cultures stimulated with the B cell mitogen, anti-CD40 antibody, showed an increase in message. In addition, co-treatment with mitogens and IL-2 uniformly caused an increase in CB1 mRNA. It is suggested that signaling pathways activated by T cell mitogens lead to decreased CB1 gene activation while pathways activated by B cell mitogens and IL-2 lead to increased CB1.
Publication types
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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 / pharmacology
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B-Lymphocytes / chemistry
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B-Lymphocytes / drug effects
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B-Lymphocytes / immunology
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CD3 Complex / immunology*
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CD40 Antigens / immunology*
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Carcinogens / pharmacology
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Female
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Gene Expression / drug effects
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Gene Expression / immunology
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Interleukin-2 / immunology
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Interleukin-2 / pharmacology*
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Mice
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Mice, Inbred BALB C
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RNA, Messenger / analysis
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Receptors, Cannabinoid
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Receptors, Drug / genetics*
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Receptors, Drug / immunology
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Signal Transduction / drug effects
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Signal Transduction / immunology
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Spleen / cytology
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Spleen / immunology
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Tetradecanoylphorbol Acetate / pharmacology
Substances
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Antibodies
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CD3 Complex
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CD40 Antigens
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Carcinogens
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Interleukin-2
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RNA, Messenger
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Receptors, Cannabinoid
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Receptors, Drug
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Tetradecanoylphorbol Acetate