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. 2020 Jan 13;33(1):3–11. doi: 10.1089/vim.2019.0076

FIG. 1.

FIG. 1.

IFN signaling pathways. Type I, type II, and type III IFNs signal through distinct receptors, but activate overlapping transcriptional programs. More than a dozen type I IFNs, including IFN-α, IFN-β, IFN-ɛ, IFN-δ, and IFN-τ, signal through a heterodimeric receptor comprising IFNAR1 and IFNAR2. A smaller set of type III IFNs (IFN-λ) signal through a heterodimeric receptor comprising IFNLR1 and IL10Rb. The type II IFN family consists only of IFN-γ, which signals as a dimer through a tetrameric receptor comprising IFNGR1 and IFNGR2. Receptor binding activates kinases, including JAK1, JAK2, and TYK2, which phosphorylate STAT1 and STAT2. Phosphorylated STATs dimerize and translocate to the nucleus, where they activate transcription from promoters that contain ISRE (STAT1/2 heterodimers) or GAS (STAT1 homodimers), resulting in the expression of IFN-stimulated genes. The canonical IFN signaling pathways are depicted, but additional signaling pathways also are activated and likely contribute to the specific transcriptional response induced by different IFNs. GAS, γ-activated sites; IFN, interferon; ISRE, IFN-stimulated response elements. Color images are available online.