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Suppresses Activation of Nuclear Transcription Factors NF-
B and Activator Protein 1 and Potentiates TNF-Induced Apoptosis1
Cytokine Research Laboratory, Department of Bioimmunotherapy, M.D. Anderson Cancer Center, University of Texas, Houston, TX 77030
We and others have reported that IFN-
potentiates the apoptotic
effects of TNF through a mechanism that is not understood. Because the
nuclear transcription factors NF-
B and AP-1 have recently been
reported to mediate anti-apoptosis and cell survival, we
hypothesized that IFN- potentiates the cytotoxic effects of TNF by
suppressing TNF-induced activation of NF-B and AP-1. We tested this
hypothesis by pretreating human Jurkat T cells with IFN-, which
blocked TNF-induced activation of NF-B and AP-1 in a time- and
dose-dependent manner as determined by EMSA. IFN- blocked
TNF-induced phosphorylation and degradation of the inhibitor subunit of
NF-B, and suppressed NF-B and AP-1 activation induced by various
other inflammatory stimuli. NF-B-dependent reporter gene expression
activated by TNF, TNFR1, TNF receptor-associated factor 2, and
NF-B-inducing kinase was also abrogated by IFN- pretreatment. The
suppression of NF-B and AP-1 correlated with the potentiation of
TNF-induced cytotoxicity and caspase activation. Overall our results
suggest that IFN- potentiates the apoptotic effects of TNF possibly
by suppressing NF-B and AP-1 activation.
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