Abstract
HIV protein gp120 in combination with T cell antigen receptor (TCR) triggering induces apoptosis (gp120-apoptosis) in Th1 cells. Gp120-apoptosis occurs by induction of Fas-L and subsequent triggering of the Fas apoptotic pathway. Here, through the use of several compounds inhibiting induction of Fas-L, we show that, in a Th1 clone, a protein kinase C (PKC) independent pathway activated by TCR stimulation is distinguishible from a PKC dependent pathway activated by either phorbol 12-myristate 13-acetate (PMA)/ionomycin or asynchronous stimulation of TCR and CD4 as occurs in gp120-apoptosis.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Antigens, Surface / genetics
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Apoptosis / drug effects
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Apoptosis / physiology*
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Cell Death / drug effects
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Cell Death / physiology
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Clone Cells
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Cyclosporine / pharmacology
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Enzyme Inhibitors / pharmacology
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Fas Ligand Protein
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Gene Expression Regulation / drug effects
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Gene Expression Regulation / physiology*
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HIV Envelope Protein gp120 / pharmacology*
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Humans
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Ionomycin / pharmacology*
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Kinetics
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Lymphocyte Activation
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Membrane Glycoproteins / biosynthesis
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Membrane Glycoproteins / genetics*
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Naphthalenes / pharmacology
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Protein Kinase C / metabolism*
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Receptors, Antigen, T-Cell / physiology
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Reverse Transcriptase Polymerase Chain Reaction
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Tetradecanoylphorbol Acetate / pharmacology
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Th1 Cells / cytology
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Th1 Cells / immunology
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Th1 Cells / physiology*
Substances
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Antigens, Surface
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Enzyme Inhibitors
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FASLG protein, human
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Fas Ligand Protein
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HIV Envelope Protein gp120
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Membrane Glycoproteins
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Naphthalenes
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Receptors, Antigen, T-Cell
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Ionomycin
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Cyclosporine
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Protein Kinase C
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calphostin C
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Tetradecanoylphorbol Acetate