Interferon-λ and interleukin 22 act synergistically for the induction of 
interferon-stimulated genes and control of rotavirus infection

Hernandez, Pedro P.; Mahlakoiv, Tanel; Yang, Ines; Schwierzeck, Vera; Nguyen, Nam; Guendel, Fabian; Gronke, Konrad; Ryffel, Bernhard; Hölscher, Christoph; Dumoutier, Laure; Renauld, Jean-Christophe; Suerbaum, Sebastian; Staehli, Peter; Diefenbach, Andreas

doi:DOI: 10.1038/ni.3180

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Interferon-λ and interleukin 22 act synergistically for the induction of interferon-stimulated genes and control of rotavirus infection

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Hernandez, Pedro P.
Research Centre Immunology and Institute of Medical Microbiology and Hygiene, University of Mainz Medical Centre;
Department of Medical Microbiology and Hygiene, Institute for Medical Microbiology and Hygiene, Freiburg University Medical Centre;
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Gronke, Konrad
Research Centre Immunology and Institute of Medical Microbiology and Hygiene, University of Mainz Medical Centre;
Department of Medical Microbiology and Hygiene, Institute for Medical Microbiology and Hygiene, Freiburg University Medical Centre;
Research Training Group (GRK1104) of Organogenesis ;
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Citation

Hernandez, P. P., Mahlakoiv, T., Yang, I., Schwierzeck, V., Nguyen, N., Guendel, F., et al. (2015). Interferon-λ and interleukin 22 act synergistically for the induction of interferon-stimulated genes and control of rotavirus infection. Nature Immunology, 16, 698-707. doi:DOI: 10.1038/ni.3180.

Cite as: https://hdl.handle.net/someHandle/test/escidoc:902517

Abstract

The epithelium is the main entry point for many viruses, but the processes that protect barrier surfaces against viral infections are incompletely understood. Here we identified interleukin 22 (IL-22) produced by innate lymphoid cell group 3 (ILC3) as an amplifier of signaling via interferon-λ (IFN-λ), a synergism needed to curtail the replication of rotavirus, the leading cause of childhood gastroenteritis. Cooperation between the receptor for IL-22 and the receptor for IFN-λ, both of which were 'preferentially' expressed by intestinal epithelial cells (IECs), was required for optimal activation of the transcription factor STAT1 and expression of interferon-stimulated genes (ISGs). These data suggested that epithelial cells are protected against viral replication by co-option of two evolutionarily related cytokine networks. These data may inform the design of novel immunotherapy for viral infections that are sensitive to interferons.