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. 2019 Aug 23;8(9):963. doi: 10.3390/cells8090963

Figure 1.

Figure 1

Signaling pathways of type I and type III interferons (IFNs). The production of (A) type I and (B) type III IFNs can be induced by virus infection or by immune complexes, which are sensed by pattern recognition receptors (PRRs), especially toll-like receptors (TLRs) and retinoic acid-inducible gene 1 (RIG-I)-like receptors (RLRs). Differential signaling molecules lead to the activation of the transcription factors nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and interferon regulatory factors (IRFs), and eventually to the activation of IFN gene transcripts. The secreted IFNs ligate to the type I or type III IFN receptors (IFN-α/β receptor (IFNAR)1/IFNAR2 or IFN-λ receptor (IFNLR)1/interleukin-10 receptor (IL-10R)2, respectively) of the neighboring cells and stimulate the production of IFN-stimulated genes (ISGs) via Janus kinase (JAK)-signal transducer and activator of transcription (STAT) pathways, which results in the production of several antiviral effectors. Cyclic GMP-AMP synthase (cGAS) transforms DNA into cyclic di-nucleotides (CDNs), which can be recognized by stimulator of interferon genes (STING). STING triggers the activation of tank-binding kinase 1 (TBK1) to phosphorylate IRF-3 and induces the transcription of type I IFNs. In the transcription of type III IFNs, the activation of STING is involved in Ku70.