We examined the direct effects of IFN-alpha on the development of Th17 with a system using immobilized anti-CD3, which permits activation of CD4+ T cells in the complete absence of accessory cells. Highly purified CD4+ T cells obtained from healthy donors were stimulated with immobilized anti-CD3 with or without IFN-alpha. IFN-alpha suppressed the production of IL-17 of immobilized anti-CD3-stimulated CD4+ T cells in a dose-response manner. Accordingly, IFN-alpha inhibited IL-17 mRNA expression in immobilized anti-CD3-stimulated CD4+ T cells. IFN-alpha did not affect the production of TGF-beta or IL-6, but inhibited RORC mRNA expression of anti-CD3-stimulated CD4+ T cells. These results indicate that IFN-alpha suppresses IL-17 expression and Th17 differentiation through down-regulation of RORC mRNA expression. It is therefore suggested that these effects might play a role in the mode of action of IFN-alpha in the treatment of various inflammatory diseases.
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