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B, Activation Protein-1, and Apoptosis1
Cytokine Research Laboratory, Department of Molecular Oncology, University of Texas M. D. Anderson Cancer Center, Houston, TX 77030
IL-13 is known to suppress the production of inflammatory cytokines
such as TNF. Whether IL-13 also modulates the biologic effects of TNF
is not known. In the present report we examined the effect of IL-13 on
TNF-induced activation of nuclear transcription factors NF-
B and
activation protein-1 (AP-1) and apoptosis. Pretreatment of cells with
IL-13 blocked TNF-induced NF-B activation, nuclear translocation of
p65 subunit, and degradation of IB
. IL-13 also inhibited
NF-B activation by LPS, okadaic acid, H2O2,
and ceramide. TNF-induced NF-B-dependent gene transcription was also
blocked by IL-13. TNF-induced activation of another nuclear
transcription factor, AP-1, was suppressed by IL-13. The activation of
N-terminal c-Jun kinase and mitogen-activated protein kinase kinase,
implicated in the regulation of AP-1 and NF-B, was also
down-regulated by IL-13. TNF-mediated cytotoxicity and activation of
caspase-3 were abolished by IL-13. The inhibitory effects of IL-13 on
TNF were sensitive to H-7, neomycin, and wortmannin, suggesting that
the pathway consisting of protein kinase C, phosphatidylinositol
3-kinase, and phospholipase C must be involved in IL-13 signaling.
Thus, overall, these results demonstrate that IL-13 is a potent
inhibitor of TNF-mediated activation of NF-B, AP-1, and apoptosis,
which may contribute to its previously described immunosuppressive and
anti-inflammatory effects.
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