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

P Accornero1, M Radrizzani, A Carè

  • 1Division of Experimental Oncology D, Istituto Nazionale Tumori, Milan, Italy.

FEBS Letters
|November 4, 1998
PubMed

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.

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