HIV GP120 AND PMA/IONOMYCIN INDUCED APOPTOSIS BUT NOT ACTIVATION-INDUCED CELL-DEATH REQUIRE PKC FOR FAS-L UP-REGULATION/

HIV protein gp120 in combination with T cell antigen receptor (TCR) tr iggering induces apoptosis (gp120-apoptosis) in Th1 cells. Gp120-apopt osis occurs by induction of Fas-L and subsequent triggering of the Fas apoptotic pathway. Here, through the use of several compounds inhibit ing induction of Fast, we show that, in a Th1 clone, a protein kinase C (PKC) independent pathway activated by TCR stimulation is distinguis hible from a PKC dependent pathway activated by either phorbol 12-myri state 13-acetate (PMA)/ionomycin or asynchronous stimulation of TCR an d CD4 as occurs in gp120-apoptosis, (C) 1998 Federation of European Bi ochemical Societies.