HIV/gp120 and PMA/ionomycin induced apoptosis but not activation induced cell death require PKC for Fas-L upregulation

FEBS Lett. 1998 Oct 9;436(3):461-5. doi: 10.1016/s0014-5793(98)01127-2.

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

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antigens, Surface / genetics
  • Apoptosis / drug effects
  • Apoptosis / physiology*
  • Cell Death / drug effects
  • Cell Death / physiology
  • Clone Cells
  • Cyclosporine / pharmacology
  • Enzyme Inhibitors / pharmacology
  • Fas Ligand Protein
  • Gene Expression Regulation / drug effects
  • Gene Expression Regulation / physiology*
  • HIV Envelope Protein gp120 / pharmacology*
  • Humans
  • Ionomycin / pharmacology*
  • Kinetics
  • Lymphocyte Activation
  • Membrane Glycoproteins / biosynthesis
  • Membrane Glycoproteins / genetics*
  • Naphthalenes / pharmacology
  • Protein Kinase C / metabolism*
  • Receptors, Antigen, T-Cell / physiology
  • Reverse Transcriptase Polymerase Chain Reaction
  • Tetradecanoylphorbol Acetate / pharmacology
  • Th1 Cells / cytology
  • Th1 Cells / immunology
  • Th1 Cells / physiology*

Substances

  • Antigens, Surface
  • Enzyme Inhibitors
  • FASLG protein, human
  • Fas Ligand Protein
  • HIV Envelope Protein gp120
  • Membrane Glycoproteins
  • Naphthalenes
  • Receptors, Antigen, T-Cell
  • Ionomycin
  • Cyclosporine
  • Protein Kinase C
  • calphostin C
  • Tetradecanoylphorbol Acetate