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. 2020 Aug 18;9(8):1913. doi: 10.3390/cells9081913

Figure 3.

Figure 3

Type I IFN synthesis pathway and production of pro-inflammatory cytokines. Virus-responsive induction of the IFN-β promoter is directed by cytoplasmic helicases RIG-I and MDA5 [74]. Intracellular RNA pathogen-associated molecular patterns (PAMPs; e.g., dsRNA) are recognized by cellular pattern recognition receptors (PRRs; e.g., RIG-I, MDA5, TLR3), triggering antiviral signalling cascades. Activation of two signalling kinases TBK-1 and IKK-ε results in phosphorylation and activation of latent IRF-3 transcription factor that is subsequently translocated to the nucleus upon dimerization [67,68]. IRF-3 binds to p300 and CBP to form the DRAF1 transcription complex for IFN-β production. Cytoplasmic V protein is known to inhibit TBK-1 driven activation of IRF-3, whereas W protein successfully inhibits both TBK-1 and IKK-ε driven activation of IRF-3, with significant effects on TIR-domain-containing adapter-inducing interferon β (TRIF)-mediated activation [29].