Skip to main content
. 2008;8(7):559–568. doi: 10.1038/nri2314

Figure 1. Interferon receptor signalling.

Figure 1

The action of the interferons (IFNs) is mediated through three receptor complexes: a heterodimer of IFNα receptor 1 (IFNAR1) and IFNAR2 binds type I IFNs; the interleukin-10 receptor 2 (IL-10R2) associates with IFNLR1 (IFNλ receptor 1) to bind the three IFNλ subtypes; and a tetramer consisting of two IFNGR2 (IFNγ receptor 2) chains and two IFNGR1 chains binds dimers of the type II IFNγ. Following binding by type I IFNs, signal transduction is initiated by pre-associated tyrosine kinases (JAK1 and TYK2 (tyrosine kinase 2)), which phosphorylate IFNAR1 and leads to the recruitment and phosphorylation of the signal transducers and activators of transcription (STATs). STAT heterodimers associate with IFN-regulatory factor 9 (IRF9) to form IFN-stimulated gene factor 3 (ISGF3), or STAT homodimers to form the IFNγ activation factor (GAF). These complexes translocate to the nucleus to induce IFN-stimulated genes from IFN-stimulated response elements (ISREs) or GAS promoter elements, for type I and type III, or type II IFN responses, respectively. Divergence from this simplified signalling pathway can occur, for example, type I IFNs are reported to elicit STAT homodimers, and more complicated interplay, with activation of other STAT proteins, occurs than is shown here. ISG15, IFN-stimulated protein of 15 kDa; Mx, myxovirus resistance; OAS, 2′,5′-oligoadenylate synthetase; PKR, protein kinase R.