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© Research
Publication : Nature immunology

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

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Nature immunology - 25 May 2015

Hernández PP, Mahlakõiv T, Yang I, Schwierzeck V, Nguyen N, Guendel F, Gronke K, Ryffel B, Hölscher C, Dumoutier L, Renauld JC, Suerbaum S, Staeheli P, Diefenbach A

Link to Pubmed [PMID] – 26006013

Nat. Immunol. 2015 Jul;16(7):698-707

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.

http://www.ncbi.nlm.nih.gov/pubmed/26006013