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HIV/gp120 and PMA/ionomycin induced apoptosis but not activation induced cell death require PKC for Fas‐L upregulation
Author(s) -
Accornero Paola,
Radrizzani Marina,
Carè Alessandra,
Mattia Gianfranco,
Chiodoni Claudia,
Kurrle Roland,
Colombo Mario P
Publication year - 1998
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(98)01127-2
Subject(s) - ionomycin , apoptosis , protein kinase c , microbiology and biotechnology , t cell receptor , fas ligand , downregulation and upregulation , phorbol , fas receptor , programmed cell death , jurkat cells , signal transduction , t cell , clone (java method) , chemistry , biology , immunology , immune system , biochemistry , dna , gene , intracellular
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.