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Fig. 7 | Virology Journal

Fig. 7

From: Interleukin-17A pretreatment attenuates the anti-hepatitis B virus efficacy of interferon-alpha by reducing activation of the interferon-stimulated gene factor 3 transcriptional complex in hepatitis B virus-expressing HepG2 cells

Fig. 7

A model of regulatory effects of IL-17A on anti-HBV activity of IFN-α. IFN-α exerts anti-HBV activity by activating JAK-STAT signaling pathway including STAT1 and STAT2 phosphorylation, transcription factor ISGF3 formation, and at last antiviral ISGs expression. Various pro-inflammatory cytokines cross-regulate the IFN-α response by altering the expression and activation of IFN-α signaling components. The pro-inflammatory function of IL-17A is primarily mediated by NF-κB signal activated by ACT1-TRAF6. In our study, IL-17A attenuates IFN-α-mediated anti-HBV activity through reduced expression and activation of ISGF3. Furthermore, IL-17A also enhances expression of negative regulators, including SOCS1/3 and USP18, inhibits expression of anti-viral ISGs and accelerates degradation of IFNAR1

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