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

被引:11
作者
Accornero, P
Radrizzani, M
Carè, A
Mattia, G
Chiodoni, C
Kurrle, R
Colombo, MP
机构
[1] Ist Nazl Tumori, Div Expt Oncol D, I-20133 Milan, Italy
[2] Ist Super Sanita, I-00161 Rome, Italy
[3] Behringwerke AG, D-3550 Marburg, Germany
关键词
human immunodeficiency virus; gp120; apoptosis; protein kinase C; Fas; CD4(+) th1 clone;
D O I
10.1016/S0014-5793(98)01127-2
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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 Fast, 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, (C) 1998 Federation of European Biochemical Societies.
引用
收藏
页码:461 / 465
页数:5
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共 41 条
[41]   CD4 and CD8: Modulators of T-cell receptor recognition of antigen and of immune responses? [J].
Zamoyska, R .
CURRENT OPINION IN IMMUNOLOGY, 1998, 10 (01) :82-87