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J Biol Chem, Vol. 274, Issue 8, 4801-4806, February 19, 1999
B by Tumor Necrosis
Factor-
and 
-Interferon in Preneuronal Cells
,
From the Tumor necrosis factor- Lineberger Comprehensive Cancer Center,
University of North Carolina School of Medicine, Chapel Hill,
North Carolina 27599, and the ¶ Department of Cancer Biology,
Lerner Research Institute, Cleveland, Ohio 44195
(TNF-) and
-interferon (IFN-) cooperate during a variety of biological
responses and ultimately synergistically enhance the expression of
genes involved in immune and inflammatory responses. Recently, we
demonstrated that IFN- can significantly potentiate TNF--induced
nuclear factor (NF)-
B nuclear translocation in neuronal derived and
endothelial cell lines. The mechanism by which these two cytokines
exert their synergistic effect on NF-B involves the de
novo degradation of the NF-B inhibitor, IB
. The
double-stranded RNA-dependent kinase PKR is IFN-inducible
and has been implicated in the activation of NF-B; therefore, we
examined the possibility that PKR may play a role in the synergistic
activation of NF-B during TNF-/IFN- cotreatment. The PKR
inhibitor 2-aminopurine (2-AP) inhibited TNF-/IFN--induced
NF-B nuclear translocation in neuronal derived cells but not in
endothelial cells. The induced degradation of IB, which is
normally observed upon TNF-/IFN- cotreatment, was blocked
completely by 2-AP in neuronal derived cells. Also, 2-AP treatment or
overexpression of a catalytically inactive PKR inhibited the
TNF-/IFN--induced synergistic activation of
B-dependent gene expression. Our results suggest that
the signal generated by IFN- during TNF-/IFN- cotreatment may
require PKR to elicit enhanced NF-B activity, and this signal may
affect the stability of the IB protein.
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