Conclusions
In vitro experiments showed that IFN-α could inhibit IL-17 expression and increased IL-10 production by PBMCs and CD4(+) T cells. The inhibitory role of IFN-α on IL-17 was partly mediated by IL-10. IFN-α activity was mediated via STAT2 phosphorylation.
Methods
Peripheral blood mononuclear cells (PBMCs) obtained from patients with active BD and controls were cultured alone or with IFN-α and the levels of IL-17 and IL-10 in the supernatants were measured by ELISA. Similar experiments were performed with isolated CD4(+) T cells from controls. The levels of phosphorylated STAT1 (p-STAT1), p-STAT2, p-STAT3 and p-STAT5 in CD4(+) T cells from controls cultured with or without IFN-α were also evaluated by ELISA. Furthermore, an experiment using anti-IL-10 was performed to examine underlying mechanisms of action of IFN-α.
Results
Significantly higher levels of IL-17 and IL-10 were observed in the supernatants of PBMCs from BD patients as compared with controls. IFN-α significantly decreased IL-17 production by PBMCs from both patients and controls. On the other hand, IFN-α increased IL-10 production by PBMCs from patients and controls. Similar findings were obtained when using CD4(+) T cells from controls, IFN-α significantly increased p-STAT2 expression in control CD4(+) T cells. Anti-IL-10 antibody was able to neutralize the inhibitory effect of IFN-α on IL-17 by 35% as compared with controls. Conclusions: In vitro experiments showed that IFN-α could inhibit IL-17 expression and increased IL-10 production by PBMCs and CD4(+) T cells. The inhibitory role of IFN-α on IL-17 was partly mediated by IL-10. IFN-α activity was mediated via STAT2 phosphorylation.