Type I interferon receptor and Type III interferon receptor (IFNAR (for Type I interferon receptor), IFNLR (for Type III interferon receptor); sometimes IFNAR1/IFNAR2 and IFNLR1/IL10R2 for their specific subunits)

Type I and Type III interferon receptors are distinct, multi-protein cell surface receptors that mediate the action of type I interferons (such as IFN-α, IFN-β) and type III interferons (IFN-λ), respectively. Both receptors play critical roles in the innate immune response, especially antiviral defense. The Type I IFN receptor consists of IFNAR1 and IFNAR2 subunits, widely expressed on most cell types, and signals via associated JAK1 and TYK2 kinases. The Type III IFN receptor (IFNLR) is comprised of IFNLR1 and IL10R2 subunits, with more restricted expression (notably epithelial cells). Ligand binding induces receptor dimerization, activation of JAK kinases, and phosphorylation of STAT transcription factors to induce expression of antiviral and immunoregulatory genes. While their intracellular signaling pathways and biological effects overlap, differences in tissue distribution and ligand-receptor binding govern their unique physiological and pathological roles. Both are validated therapeutic targets, with recombinant interferons and receptor modulators in clinical and investigational use.

Other names

IFNARinterferon alpha/beta receptorIFNAR1/IFNAR2 complexIFNLRinterferon lambda receptorIFNLR1/IL10R2 complex

Activation of JAK-STAT signaling pathway following interferon binding, leading to phosphorylation of STAT proteins, dimerization, and translocation to the nucleus to activate ISGs. Antiviral activity, immune modulation, and antiproliferative effects via upregulation of ISGs