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The Journal of Immunology, 2000, 165: 5472-5479.
Copyright © 2000 by The American Association of Immunologists

IFN-{gamma} and IFN-{alpha} Posttranscriptionally Down-Regulate the IL-4-Induced IL-4 Receptor Gene Expression1

Eui-Young So, Hyun-Hee Park and Choong-Eun Lee2

Department of Biological Science and Institute for Basic Science, SungKyunKwan University, Suwon, Korea

As Th1 and Th2 cytokines, IFN-{gamma}/{alpha} and IL-4 counterregulate diverse immune functions. In particular, IFN-{gamma} and IFN-{alpha} have been reported to markedly suppress the IL-4-induced IgE production and type II IgE receptor (Fc{epsilon}RII/CD23) expression. Because modulation of IL-4R may be an important mechanism in the regulation of IL-4 response, we have investigated the effect of IFN-{gamma}/{alpha} on IL-4R expression and signal transduction mechanisms involved in this process. In human mononuclear cells and B cells isolated from tonsil or peripheral blood, IL-4 up-regulates IL-4R({alpha}) expression at surface protein and mRNA levels, and the IL-4-induced IL-4R({alpha}) is significantly down-regulated by both IFN-{gamma} and IFN-{alpha} to a similar extent. The inhibitory effects of IFN-{gamma}/{alpha} on the IL-4R mRNA expression require a lag period of about 8 h, and are sensitive to cycloheximide treatment, which suggests that the suppressive effect of IFNs on IL-4R gene expression is a secondary response requiring de novo synthesis of IFN-induced factors. Under such conditions that the inhibitory effects of IFNs are observed, IFNs do not affect the IL-4-induced STAT6 activation and IL-4R transcription, as analyzed by EMSA and nuclear run-on assays, respectively. Subsequently, mRNA stability studies have indicated that the action of IFN-{gamma}/{alpha} is primarily mediated by an accelerated decay of IL-4-induced IL-4R mRNA. Thus, it appears that, as already shown in the case of the IL-4-induced Fc{epsilon}RII regulation, posttranscriptional inhibition of IL-4-inducible genes by mRNA destabilization is a common mechanism by which type I and II IFNs antagonize the IL-4 response in human immune cells.




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