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. Copyright (C) 1998 Federation of European Biochemical Societies.
Original language | English |
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Pages (from-to) | 461-465 |
Number of pages | 5 |
Journal | FEBS Letters |
Volume | 436 |
Issue number | 3 |
DOIs | |
Publication status | Published - Oct 9 1998 |
Keywords
- Apoptosis
- CD4 Th1 clone
- Fas
- gp120
- Human immunodeficiency virus
- Protein kinase C
ASJC Scopus subject areas
- Biochemistry
- Biophysics
- Molecular Biology