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      IFN-lambdas mediate antiviral protection through a distinct class II cytokine receptor complex.

      Nature immunology
      Cell Line, Amino Acid Sequence, Animals, Antiviral Agents, metabolism, Base Sequence, COS Cells, Chromosomes, Human, Pair 19, genetics, Cloning, Molecular, DNA, Complementary, Humans, Interferons, classification, Interleukin-10 Receptor beta Subunit, Ligands, Macromolecular Substances, Membrane Glycoproteins, Molecular Sequence Data, Receptors, Cytokine, Recombinant Proteins, Sequence Homology, Amino Acid, Signal Transduction, Virus Diseases, immunology

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          Abstract

          We report here the identification of a ligand-receptor system that, upon engagement, leads to the establishment of an antiviral state. Three closely positioned genes on human chromosome 19 encode distinct but paralogous proteins, which we designate interferon-lambda1 (IFN-lambda1), IFN-lambda2 and IFN-lambda3 (tentatively designated as IL-29, IL-28A and IL-28B, respectively, by HUGO). The expression of IFN-lambda mRNAs was inducible by viral infection in several cell lines. We identified a distinct receptor complex that is utilized by all three IFN-lambda proteins for signaling and is composed of two subunits, a receptor designated CRF2-12 (also designated as IFN-lambdaR1) and a second subunit, CRF2-4 (also known as IL-10R2). Both receptor chains are constitutively expressed on a wide variety of human cell lines and tissues and signal through the Jak-STAT (Janus kinases-signal transducers and activators of transcription) pathway. This receptor-ligand system may contribute to antiviral or other defenses by a mechanism similar to, but independent of, type I IFNs.

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